Pain Cancer Research Results

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Type:

Pain

Scientific Papers found: Click to Expand⟱

5323-

ALC,

Preventive Effect of Acetyl-L-carnitine on Oxaliplatin-induced Peripheral Neuropathy

Trial,

Var,

Pain↓, Studies have shown that acetyl-L-carnitine can improve the energy metabolism of neurotransmitters and inhibit the release of glutamine in the intersynaptic space to reduce pain.
NP/CIPN↓, Some small model studies have also found that acetyl-L-carnitine has a definite therapeutic effect on peripheral neurological lesions induced by chemotherapy.

5427-

ASTX,

Astaxanthin and Cancer Chemoprevention

Review,

Var,

chemoP↑, evidence for anticarcinogenic behavior of selected carotenoids, with an emphasis on the chemopreventive activities of astaxanthin.
AntiCan↑, Human epidemiological studies have revealed a protective effect of vegetable and fruit consumption for cancers of the stomach, esophagus, lung, oral cavity and pharynx, bladder, endometrium, pancreas, colon and rectum, breast, cervix, ovary and prost
chemoPv↑, the chemopreventive effects of canthaxanthin
Risk↓, Salmon, the principal dietary source of astaxanthin, is an important component of the traditional diets of Eskimos and certain coastal tribes in North America; these groups have shown unusually low prevalence of cancer.
lipid-P↓, Dietary astaxanthin also reduced metastatic nodules and lipid peroxidation in the livers of rats treated with restraint stress.
Pain↓, The results revealed that astaxanthin significantly relieved pain and improved performance in patients with RA
BioAv↑, the results demonstrated an enhancement of astaxanthin bioavailability in humans when incorporated into lipid-based formulations.
Dose↝, relevant dietary dosages of astaxanthin (4-12 mg daily is typically recommended by supplement manufacturers),

5370-

AV,

The Effect of Aloe Vera Solution on Chemotherapy-Induced Stomatitis in Clients with Lymphoma and Leukemia: A Randomized Controlled Clinical Trial

Trial,

AML,

Dose↝, The intervention group patients were asked to wash their mouths with 5 ml of aloe vera solution for two minutes three times a day for 14 days.
stomatitis↓, However, a significant difference was observed between the two groups in this regard on other days (days 3-14: P=0.001 for stomatitis intensity, P=0.001 for pain).
Pain↓,

6510-

BCP,

CBD,

Cannabidiol and Beta-Caryophyllene Combination Attenuates Diabetic Neuropathy by Inhibiting NLRP3 Inflammasome/NFκB through the AMPK/sirT3/Nrf2 Axis

in-vivo,

Nor,

BC (30 mg/kg), CBD (15 mg/kg)

Rats

*MMP↓, BC and CBD diminished HG-induced hyperglycemia in Schwann cells, in part by reducing mitochondrial membrane potential, reactive oxygen species, and mitochondrial superoxides.
*ROS↑,
*BloodF↑, while improving blood flow
*Pain↓, CBD and BC treatments also reduced pain hypersensitivity to hyperalgesia and allodynia, with increased antioxidant and anti-inflammatory action in diabetic rats.
*antiOx↑,
*Inflam↓,
*AMPK↑, in vivo effects were attributed to significant upregulation of AMPK, sirT3, Nrf2, PINK1, PARKIN, LC3B, Beclin1, and TFAM functions
*SIRT3↑,
*NRF2↑,
*PINK1↑,
*PARK2↑,
*LC3B↑,
*Beclin-1↑,
*TFAM↑,
*NLRP3↓, while downregulation of NLRP3 inflammasome, NFκB, COX2, and p62 activity was noted
*NF-kB↓,
*COX2/PTGS2↓,
*p62↓,
*NP/CIPN↓, CBD and BC combination ameliorates DN by modulating the mitochondrial quality control system.

6503-

BCP,

The Potential Therapeutic Role of Beta-Caryophyllene as a Chemosensitizer and an Inhibitor of Angiogenesis in Cancer

Review,

Var,

ChemoSen↑, Beta-Caryophyllene (BCP), was highlighted in several recent preclinical studies to enhance chemo-sensitization in chemo-resistant tumors and to efficiently inhibit angiogenesis and cancer cells’ ability to invade and metastasize.
angioG↓,
TumCI↓,
TumMeta↓,
ROS↑, BCP seems to work as a dual modulator of oxidative stress, increasing reactive oxygen species (ROS) in cancer cells, and thus enhancing apoptosis, but reducing ROS in normal cells to protect them from damage
*ROS↓,
chemoP↑,
CB2 / CNR2↑, important issue in BCP is its ability to bind to the body’s cannabinoid receptor 2 (CB2), where it binds selectively to the CB2 receptors and not the CB1 receptor, which makes it non-psychoactive and therapeutically appealing.
Inflam↓, activation of the CB2 receptor by BCP can suppress pro-inflammatory cytokines production, helping to create an anti-tumor immune environment
AntiTum↑,
*BioAv↑, Beta-Caryophyllene, a food additive approved by the Food and Drug Administration, is efficiently absorbed in the gastro-intestinal tract and can penetrate the blood–brain barrier and has a well-established safety profile, making it an attractive biom
*BBB↑,
Apoptosis↑, Induces apoptosis and suppresses proliferative activity of lung cancer cells
TumCP↑,
TumCCA↑, Induces G1 cell cycle arrest by dysregulating cyclins and other molecules
RadioS↑, GBM: Works as a potential radiosensitizer for improving RT outcomes by inhibiting DNA repair, inducing apoptosis, and suppressing anti-apoptotic and survival pathways
DNArepair↓,
ROS↑, BC: Enhances sensitization and promotes the cigarette smoke condensate (CSC)-induced apoptosis in MDA-MB-468 cells, mainly by triggering oxidative stress and inhibition of STAT3
STAT3↓,
*BioEnh↑, BCP is considered a key component in black pepper’s ability to enhance nutrient absorption, including compounds like curcumin.
Pain↓, BCP in cloves further supports their role in pain management and infection prevention.
AntiBio↓,
ROS↑, selectively induce apoptosis and oxidative stress in cancer cells while sparing normal cells at lower concentrations.
Dose↝, I50, for many cancer cell lines typically ranges from 19 to 64 μM
NF-kB↓, Beta-Caryophyllene was reported to inhibit the central to the regulators of inflammation, NF-κB and MAPK pathways, leading to a decrease in pro-inflammatory cytokine (TNF-α, IL-1β, and IL-6) production
MAPK↓,
TNF-α↓,
IL1β↓,
IL6↓,
cl‑PARP↑, through increasing the levels of cleaved PARP, caspases and Bax, and the downregulation of Bcl-2, directly by interaction with CB2.
Casp↑,
BAX↑,
Bcl-2↓,
VEGF↓, BCP blocks migration of endothelial cells by inhibiting the secretion of VEGF, and thus blocking the activity of the tyrosine kinase VEGFR2
VEGFR2/KDR/Flk1↓,
MMP2↓, BCP can also prohibit the secretion of MMP-2, p-p38 and p-ERK
p‑p38↓,
p‑ERK↓,
EPR↑, BCP was suggested to accumulate in the cancer cell membrane, altering the cells’ permeability, leading to the accumulation of anticancer drugs, and consequently strengthening the drugs’ activity.
P-gp/ABCB1↓, direct inhibition of P-glycoprotein (P-gp/ABCB1) and multidrug resistance-associated protein 1 (MRP1/ABCC1), which are overexpressed in resistant tumors
MRP1/ABCC1↓,
*NRF2↑, Importantly, BCP’s selective antioxidant activity—activating Nrf2 in normal cells while increasing ROS in cancer cells—minimizes off-target toxicity,
*antiOx↑,

6508-

BCP,

The CB2 Agonist β-Caryophyllene in Male and Female Rats Exposed to a Model of Persistent Inflammatory Pain

in-vivo,

Nor,

rats

*Pain↓, long-term intake of BCP appears to be able to decrease pain behaviors in a model of repeated inflammatory pain in both sexes, but to a greater degree in males.

5680-

BML,

Anticancer properties of bromelain: State-of-the-art and recent trends

Review,

Var,

*Inflam↓, anticancer, anti-edema, anti-inflammatory, anti-microbial, anti-coagulant, anti-osteoarthritis, anti-trauma pain, anti-diarrhea, wound repair.
*Bacteria↓,
*Pain↓,
*Diar↓,
*Wound Healing↑,
ERK↓, Figure 1
JNK↓,
XIAP↓,
HSP27↓,
β-catenin/ZEB1↓,
HO-1↓,
lipid-P↓,
ACSL4↑,
ROS↑,
SOD↑,
Catalase↓,
GSH↓,
MDA↓,
Casp3↓,
Casp9↑,
DNAdam↑,
Apoptosis↑,
NF-kB↓,
P53↑,
MAPK↓,
APAF1↑,
Cyt‑c↓,
CD44↓,
Imm↑, Bromelain was also studied in the innate immune system, where it could enhance and sustain the process
ATG5↑,
LC3I↑,
Beclin-1↑,
IL2↓, bromelain in vitro experiments resulted in diminished amounts of IL-2, IL-6, IL-4, G-CSF, Gm-CSF, IFN-γ,
IL4↓,
IFN-γ↓,
COX2/PTGS2↓, proprietary bromelain extract could decrease IL-8, COX-2, iNOS, and TNF-α without affecting cell viability.
iNOS↓,
ChemoSen↑, Bromelain may increase the cytotoxicity of cisplatin in the treatment of breast cancer as reported in 2 studies with MDA-MB-231 and 4T1 Breast Tumor cell lines
RadioS↑, The size and weight of tumors in gamma-irradiated EST-bearing mice treated with bromelain decreased significantly with a significant amelioration in the histopathological examination
Dose↝, oral bromelain administration in breast cancer patients (daily up to a dose of 7800 mg)
other↓, The role of bromelain (in combination with papain, sodium selenite and Lens culinaris lectin) has been also tested as a complementary medicine on more than 600 breast cancer patients to reduce the side effects caused by the administration of the adju

5661-

BNL,

A clinical and mechanistic study of topical borneol‐induced analgesia

Trial,

Nor,

double‐blind, placebo‐controlled clinical study involving 122 patients with postoperative pain.

*Pain↓, Topical application of borneol led to significantly greater pain relief than placebo did.

6542-

BSB,

Health Benefits, Pharmacological Effects, Molecular Mechanisms, and Therapeutic Potential of α-Bisabolol

Review,

Var,

Review,

Park,

Review,

AD,

AntiCan↑, Numerous experimental studies demonstrated pharmacological properties of α-Bisabolol including anticancer, antinociceptive, neuroprotective, cardioprotective, and antimicrobial.
*neuroP↑,
*cardioP↑,
*AntiBio↑,
*BioAv↑, Given the polypharmacological effects and pleiotropic properties, along with favorable pharmacokinetics, and dietary availability and safety, α-Bisabolol can be used as a dietary agent, nutraceutical or phytopharmaceutical agent or as an adjuvant wit
*toxicity↓,
*BioAv↑, integrated in many cosmetic formulations due to its skin soothing effects, well documented dermal absorption
*motorD↑, improvement in locomotor activity, a reduction in the expression of thiol and a reinstate of the activity of mitochondrial complex-I.
*SOD↑, α-Bisabolol also increased the mRNA level of antioxidants proteins such as superoxide dismutase (SOD), catalase (CAT), and the keap1 gene product.
*Catalase↑,
*Keap1↑,
*MDA↓, α-Bisabolol attenuated oxidative insult by reducing malondialdehyde (MDA), restoring depleted glutathione (GSH) and improving SOD and CAT activity.
*GSH↑,
*IL1β↓, attenuated neuroinflammation by reducing glial cells activation and subsequent release of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) and mediators (iNOS and COX-2).
*IL6↓,
*TNF-α↓,
*iNOS↓,
*COX2/PTGS2↓,
*lipid-P↓, α-Bisabolol restored mitochondrial function by preventing mitochondrial lipid peroxidation, cytochrome-C release and most importantly preserving Complex-I activity
*Cyt‑c↓,
*ROS↓, The study concluded that α-Bisabolol safeguarded against the induced upsurge of ROS and nitrite.
*MMP↑, α-Bisabolol treatment also restored mitochondrial membrane potential (MMP) validating its antioxidant effect.
*antiOx↑,
*AChE↓, showed a significant reduction in AChE activity and an ability to avert Ach depletion.
*Apoptosis↓, α-Bisabolol protected cells from Aβ triggered apoptosis by reducing Bax and Caspase-3 and increasing Bcl-2 activity.
*BAX↓,
*Casp3↓,
*Bcl-2↑,
*BACE/β-secretase↓, α-Bisabolol inhibitory activity on BACE1 and found a decrease in BACE1 activity following α-Bisabolol treatment
*BChE↓, AChE, BuChE, β-secretase actions were decreased significantly in cells pretreated with α-Bisabolol
*eff↑, The compound clearly illustrated a potent anti-AchE activity of 95.869% similar to the activity of donepezil, a standard drug. I
*Aβ↓, The compound also disaggregated Aβ25–35 peptide and protected against its induced toxicity by increasing neuro2a cells viability [
*ATP↑, figure 2
RadioS↑, α-Bisabolol and Anticancer Effects, figure 3
Cyt‑c↑,
Casp3↑,
Casp8↑,
Casp9↑,
Apoptosis↑,
PARP↑,
BAX↑,
BID↑,
NF-kB↑,
Fas↑,
EGFR↑,
TIMP2↑,
XIAP↓,
COX2/PTGS2↓,
Bak↓,
Bcl-2↓,
P53↑, The expression of p53 (a transcription factors whose products might lead to apoptosis), NF-κB and Fas was increased following α-Bisabolol treatment, indicating their function in mediating α-Bisabolol-induced apoptosis in the cancer cell line.
HER2/EBBR2↓,
FGF↓,
CEA↓,
Akt↓,
TumCCA↑, α-Bisabolol suppresses the cellular proliferation at G2/M cell cycle phase.
*Imm↑, reported that α-Bisabolol boosted the immunity response by T-cell subsets (CD4 and CD8) supplementation in treated mice.
*CD4+↑,
*CD8+↑,
*BBB↑, ↑ BBB penetration
*Pain↓, α-Bisabolol based mouthwash to that of chlorhexidine in reducing pain during brushing
*cardioP↑, α-Bisabolol and Cardioprotection, figure 5
*TBARS↓, rats co-treated with α-Bisabolol showed reduced LOOH and TBARS and increased SOD, CAT and GSH.
*SOD↑,
*Catalase↑,
*GSH↑,
*AntiBio↑, α-Bisabolol demonstrated an antibacterial effect against Staphylococcus aureus, Escherichia coli and Pseudomonas aeruginosa as well as a synergism against S. aureus, when combined with the antibiotic norfloxacin and against E. coli when combined with
*AntiFungal↑, ↓ fungal growth
*GastroP↑, α-Bisabolol and Gastroprotection. oral administration of α-Bisabolol was realized to attenuate gastric damage and to provide cytoprotection in stomach.
*RenoP↑, The nephroprotective effects of α-Bisabolol and the underlying mechanisms are summarized in Table 10.
*creat↓, ↓ creatinine, urea, uric acid
*uricA↓,
*Inflam↓, Anti-Inflammatory Effects of α-Bisabolol
*iNOS↓, ↓ iNOS, COX-2, TNF-α, p65 PGE2, nitrite, IL-6, ↓ MMP13
*COX2/PTGS2↓,
*TNF-α↓,
*IL6↑,
*MMP13↓,

5741-

Buty,

Rad,

Microencapsulated Sodium Butyrate in the Prevention of Acute Radiotherapy Proctitis: Single-Center Prospective Study

in-vivo,

Pca,

122 consecutive patients with prostate cancer treated in Radiotherapy

Dose↝, treatment with micro-encapsulated sodium butyrate (MESB) (3 tablets/day). (600 mg of butyrate), a dosage recommended by the manufacturer (Butyrose® Lsc Microcaps-EP2352386B1, BLM, Sila Srl, Noale (VE), Italy).
radioP↑, MESB appears effective in reducing radiation-induced bowel toxicity during RT, minimizing stool changes, incontinence, and abdominal pain.
Pain↓,

5842-

CAP,

Capsaicin: Current Understanding of Its Mechanisms and Therapy of Pain and Other Pre-Clinical and Clinical Uses

Review,

Nor,

Review,

Diabetic,

*Pain↓, capsaicin promotes pain relief when used in the right dosage and frequency.
*TRPV1↑, capsaicin-induced pain is also used to assess new molecules that target TRPV1 receptor. Capsaicin activates TRPV1
AMPK↑, The inhibitory effect of capsaicin on this process seems to involve the activation of 5’ adenosine monophosphate-activated protein kinase (AMPK) in conjunction with intracellular ROS release
ROS↑,
TumCP↑, AMPK activation is also linked to inhibition of cell proliferation and apoptosis [153,154]
Apoptosis↑,
TumCCA↑, capsaicin targets preadipocyte proliferation by blocking the S-phase of the cell cycle [149].
Casp3↑, capsaicin induces apoptosis in preadipocytes via the activation of caspase-3, Bax, and Bak, cleavage of PARP, and down-regulation of Bcl-2
BAX↑,
Bak↑,
cl‑PARP↑,
Bcl-2↓,
RNS↑, capsaicin induces apoptosis in BMSC via increased production of ROS and reactive nitrogen species (RNS) [
*glucose↓, healthy male volunteers revealed that capsaicin lowers glucose and increases insulin levels shortly after oral administration
*Insulin↑,
*BP↓, Capsaicin stimulates the release of CGRP through the activation of TRPV1 and therefore decreases blood pressure
*AntiAg↑, Capsaicin has been shown to inhibit platelet aggregation [199,200], which may also provide protection against cardiovascular diseases
ER Stress↑, endoplasmic reticulum stress in human nasopharyngeal carcinoma and pancreatic cancer cells,
Hif1a↓, capsaicin increases the degradation of hypoxia inducible factor 1α in non-small cell lung cancer,
chemoPv↑, mounting evidence supporting a chemo-preventive role for capsaicin in cancer cell culture and animal models,

5832-

CAP,

Capsaicin induces cell cycle arrest and apoptosis in human KB cancer cells

in-vitro,

Oral,

50, 100, 150, 200 and 250 μM

TumCP↓, apsaicin significantly reduced cell proliferation/viability and induced cell death in a dose-dependent manner compared with that in the untreated control.
tumCV↓,
TumCCA↑, Cell cycle analysis indicated that exposure of KB cells to capsaicin resulted in cell cycle arrest at G2/M phase.
Apoptosis↑, Capsaicin-induced growth inhibition of KB cells appeared to be associated with induction of apoptosis.
MMP↓, Moreover, capsaicin induced disruption of the mitochondrial membrane potential as well as activation of caspase 9, 3 and poly-(ADP-ribose) polymerase in KB cells.
Casp9↑,
Casp3↑,
PARP↑,
Inflam↓, capsaicin can relieve inflammation and pain associated with some diseases and cancer
Pain↓,

5831-

CAP,

Unraveling TRPV1’s Role in Cancer: Expression, Modulation, and Therapeutic Opportunities with Capsaicin

TRPV1↑, Activation of TRPV1 triggers calcium influx and affects cell signaling linked to growth and death.
Ca+2↑,
AntiCan↑, Capsaicin has been extensively studied for its anti-cancer effects, such as inhibiting cell proliferation and modulating cancer-related pain.
TumCP↓,
Pain↓,
TumCG↓, reduced tumor growth and enhanced chemosensitivity, positioning it as a promising adjunct in cancer therapy
ChemoSen↑, Capsaicin sensitizes cancer cells to chemotherapy drugs, thereby improving therapeutic outcomes [25]
Apoptosis↑, apsaicin-induced TRPV1 activation triggers apoptosis in colorectal cancer cells through the calcineurin–NFAT2–p53 signaling pathway [39]
ROS↑, Increased intracellular calcium from TRPV1 activation causes mitochondrial overload, leading to disrupted function, elevated ROS, loss of membrane potential, and cytochrome C release [Figure 2].
MMP↓,
Cyt‑c↑,
Casp↑, This triggers caspase activation and cell death.

5825-

CAP,

Bioavailability of capsaicin and its implications for drug delivery

Review,

Var,

Review,

Arthritis,

Review,

Obesity,

*AntiCan↑, Emerging studies show that it displays potent anti-tumor activity in several human cancers.
*TRPV1↑, The “heat-sensation” of capsaicin arises due to the binding of capsaicin to transient receptor potential vanilloid (TRPV) ion-channel receptors
*cardioP↑, some of the biological activities of capsaicin, like its anti-neoplastic, cardioprotective effects, have been found to be independent of the TRPV1 receptor.
AntiCan↓, Exposure to high doses of capsaicin (above 100 mg capsaicin per kg body weight) for a prolonged time causes peptic ulcers, accelerates the development of prostate, stomach, duodenal, and liver cancers and enhances breast cancer metastasis [5, 6].
Apoptosis↑, Capsaicin induces robust apoptosis in multiple types of human cancer cells both in vitro and in mice models.
ChemoSen↑, Capsaicin potentiates the apoptotic activity of cisplatin in human stomach cancer and attenuates cisplatin-induced renal toxicity in rodent models
*Inflam↓, oral or local administration of capsaicin reduces inflammation and pain from rheumatoid arthritis, fibromyalgia and chemical hyperalgesia
*Pain↓,
*AntiAg↑, The anti-platelet and anti-coagulant activity of capsaicin was independent of TRPV1
*Weight↓, capsaicinoids show anti-obesity activity by enhancing energy expenditure of the body
*BioAv↑, Capsaicin is robustly absorbed from the skin upon topical administration [4]
BioAv↑, capsaicin is rapidly absorbed from the stomach and the intestine following oral administration.
Half-Life↝, The liver and kidney displayed maximal amounts of capsaicin in 3 hours and 6 hours, respectively.
Half-Life↓, An interesting fact to note is that the bioavailability and half-life of capsaicin is quite low in the plasma, irrespective of the route of administration.

5829-

CAP,

Anti-cancer activity of capsaicin and its analogs in gynecological cancers

Review,

Var,

Pain↓, It is a potent pain-relieving agent and is often present in over-the-counter analgesic lotions and creams.
BioAv↓, clinical development of capsaicin as a viable anti-cancer drug has remained challenging due to its poor bioavailability and aqueous solubility properties.
toxicity↝, the administration of capsaicin is associated with adverse side effects like gastrointestinal cramps, stomach pain, irritation in the gut, nausea diarrhea and vomiting.
toxicity↓, The design of selective non-pungent capsaicin analogs and capsaicin-based polymeric drug delivery systems may foster the hope of novel strategies for the treatment and management of gynecological cancers.

5827-

CAP,

The Effect of Topical Capsaicin 8% on Pain in Chemotherapy-induced Peripheral Neuropathy

Trial,

Var,

17 patients,

Pain↓, For 9 patients (53%), pain became “acceptable” at t2 and t3, with a significant reduction (pain intensity difference
NP/CIPN↓,
Dose↝, Topical capsaicin 8% is a valuable treatment for pain in chemotherapy-induced peripheral neuropathy for many patients.
TRPV1↑, Capsaicin is a selective agonist of the transient receptor potential (cation channel) vanilloid, subfamily member 1 (TRPV1).
Ca+2↑, When TRPV1 is activated, this leads to calcium influx, enhancing nociception.

5860-

CAP,

Beneficial Effects of Capsaicin in Disorders of the Central Nervous System

Review,

AD,

Review,

Park,

Review,

Stroke,

*neuroP↑, In Alzheimer’s disease, capsaicin reduces neurodegeneration and memory impairment.
*memory↑, dietary capsaicin (0.01% in a chow) improved memory in a mouse model of Alzheimer’s disease
*Pain↓, Additionally, this compound exerts pain-relieving effects in migraine and cluster headaches.
*TRPV1↑, capsaicin stimulates TRPV1 receptors
*Aβ↓, Alzheimer’s disease, that dietary capsaicin (0.01% in a chow) reduced beta-amyloid plaque formation and tau phosphorylation in different brain areas
*tau↓,
*cognitive↑, attenuated neurodegeneration and cognitive impairment
*Risk↓, In western regions of China, chili peppers are more often consumed and there is a smaller number of people with dementia than in other regions where dietary capsaicin intake is lower
*motorD↓, capsaicin reduced neurodegeneration and motor impairment in animal models of Parkinson’s disease
*ROS↓, this compound decreased the production of reactive oxygen species and proinflammatory cytokines (TNF-α and IL-β) by activated microglia
*TNF-α↓,
*IL1β↓,
*eff↑, Capsaicin exerts beneficial effects in stroke models not only by enhancing neuroprotection but also by influencing cerebral vasculature.
*Risk↓, Moreover, it was reported that dietary capsaicin (0.02% in a chow) delays the onset of stroke in stroke-prone rats with hypertension.

5855-

CAP,

Unravelling the Mystery of Capsaicin: A Tool to Understand and Treat Pain

in-vivo,

Nor,

NP/CIPN↓, For example, the 8% patch is currently used in the treatment of localized neuropathic conditions, such as postherpetic neuralgia (PHN).
BioAv↑, Because capsaicin is not water-soluble, alcohols and other organic solvents are used to solubilize capsaicin in topical preparations and sprays.
Half-Life↑, Capsaicin levels declined very rapidly, with a mean population elimination half-life of 1.64 h.
TRPV1↑, Rapid desensitization first involves capsaicin binding of TRPV1
Pain↓, hese studies suggest that a high-dose patch of capsaicin has tolerable efficacy in patients with a localized pain as a result of nerve injury
TRPV1↑, agents acting on TRPV1 receptors, as well as capsaicin itself,

5881-

CAR,

Carvacrol—A Natural Phenolic Compound with Antimicrobial Properties

Review,

Nor,

*Bacteria↓, Carvacrol, either alone or in combination with other compounds, has a strong antimicrobial effect on many different strains of bacteria and fungi that are dangerous to humans
*Inflam↓, Carvacrol also exerts strong anti-inflammatory properties by preventing the peroxidation of polyunsaturated fatty acids by inducing SOD, GPx, GR, and CAT, as well as reducing the level of pro-inflammatory cytokines in the body.
*SOD↑,
*GPx↑,
*GSR↑,
*Catalase↑,
*toxicity↓, Carvacrol is considered a safe compound despite the limited amount of data on its metabolism in humans.
*Pain↓, carvacrol has been used as a substitute for cretol and carbolic acid in the treatment of toothache, sensitive dentine, and alveolar abscess, and as an antiseptic in the pulp canals of the teeth
*other↑, because it has much greater activity as a mosquito repellent than the commercial preparation, N,N-diethyl-m-methylbenzamide
*cardioP↑, other biological activities, including cardio-, reno-, and neuroprotective [20]; immune response-modulating [21]; antioxidant; anti-inflammatory [22];
*RenoP↑,
*neuroP↑,
*antiOx↑,
*AntiDiabetic↑, antidiabetic; hepatoprotective [28]; and anti-obesity properties
*hepatoP↑,
*Obesity↓,
*AntiAg↑, figure 1
*BioAv↓, challenges surrounding the wider use of carvacrol in food or feed are its unpleasant and pungent taste at higher doses; low bioavailability;
BioAv↝, sensitivity to the surrounding environment, such as in processing conditions (e.g., heat or other ingredients); and the acidic environment in the digestive tract.
*OS↑, pneumonia. Administration of carvacrol to mice (10, 25, 50 mg/kg) was associated with increased survival and significantly reduced bacterial load
MMP↓, carvacrol was found to cause greater membrane depolarization and increased oxidative stress in E. coli cells;
ROS↑,
*MDA↓, In studies conducted in guinea pigs, carvacrol concentrations of 120 and 240 μg/mL have been shown to reduce malondialdehyde levels compared to the control group
*lipid-P↓, Carvacrol prevents lipid peroxidation by inducing SOD, GPx, GR, and CAT [85,86].
*COX2/PTGS2↓, A decrease in COX-2 gene expression was found at carvacrol concentrations of 0.008% and 0.016%
*Dose↝, Phase I clinical trial, carvacrol was administered to healthy subjects at 1 and 2 mg/kg/day for 1 month, and no critical adverse reactions

5888-

CAR,

Therapeutic application of carvacrol: A comprehensive review

Review,

Var,

Review,

Stroke,

Review,

Diabetic,

Review,

Park,

*antiOx↑, demonstrated as anti‐oxidant, anticancer, diabetes prevention, cardioprotective, anti‐obesity, hepatoprotective and reproductive role, antiaging, antimicrobial, and immunomodulatory properties.
*AntiCan↑,
*AntiDiabetic↑,
*cardioP↑,
*Obesity↓,
*hepatoP↑,
*AntiAg↑,
*Bacteria↓,
*Imm↑,
MMP2↓, anticancer ability against malignant cells via decreasing the expressions of matrix metalloprotease 2 and 9, inducing apoptosis
MMP9↓,
Apoptosis↓,
MMP↓, disrupting mitochondrial membrane, suppressing extracellular signal‐regulated kinase 1/2 mitogen‐activated protein kinase signal transduction
ERK↓,
PI3K↓, decreasing the phosphoinositide 3‐kinase/protein kinase B.
ALAT↓, decreased the concentrations of alanine aminotransferase, alkaline phosphatase and aspartate aminotransferase,
*ROS↓, Essential oils found in plants are natural anti‐oxidants that reduce cell damage caused by reactive species and prevent mutagenic and carcinogenic processes.
*Catalase↑, Carvacrol has remarkably higher anti‐oxidative and hepatoprotective properties, which improves the activity of enzymatic anti‐oxidants (catalase, superoxide dismutase, and glutathione peroxidase)
*SOD↑,
*GPx↑,
*AST↓, Carvacrol decreased the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactic acid dehydrogenase (LDH) and improved the status of inflammation, necrosis, and coagulation in the liver
*LDH↓,
*necrosis↓,
ROS↑, prostate cancer cells via lowering cell viability, increasing the rate of reactive oxygen species, and disrupting the mitochondrial membrane potential.
TumCCA↑, Carvacrol induced cell cycle arrest at G0/G1 that declined increased CDK inhibitor p21 expression and decreased cyclin‐dependent kinase 4 (CDK4), and cyclin D1 expressions.
CDK4↓,
cycD1/CCND1↓,
NOTCH↓, carvacrol inhibited Notch signaling in PC‐3 cells via downregulating Jagged‐1 and Notch‐1
IL6↓, human prostate cancer cell lines, which significantly reduced IL‐6
chemoP↑, Carvacrol has significant protective effects in reducing the side effects of chemotherapeutics such as irinotecan hydrochloride anticancer drugs that cause induction of intestinal mucositis.
*Pain↓, Pain management
*neuroP↑, The neuroprotective role of carvacrol was examined by Guan et al. in 2019 against ischemic stroke,
*TRPM7↓, downregulating TRPM7 channels
*motorD↑, improved catalepsy, akinesia, bradykinesia, locomotor activity, and motor coordination.
*NF-kB↓, Carvacrol reduced inflammatory biomarkers, such as nuclear factor κB and cyclooxygenase‐2, and levels of nitric oxides, malondialdehyde, and glutathione create oxidative stress.
*COX2/PTGS2↓,
*MDA↓,

5926-

CAR,

An Updated Review of Research into Carvacrol and Its Biological Activities

Review,

Nor,

Review,

AD,

Review,

Asthma,

*Inflam↓, ic, analgesic, anti-inflammatory,antioxidant, and neuroprotective effects.
*antiOx↑,
*neuroP↑, Carvacrol has exhibited notable neuroprotective effects in experimental models of cognitiveimpairment and neurodegenerative diseases
*BioAv↑, advances in encapsulation andnanotechnology have enhanced its stability and bioavailability
*toxicity↓, Compared to phenol, carvacrol and thymol exhibitsignificantly lower toxicity. This makes carvacrol a safer alternative for various applications, frombiological agents to dietary supplements [
*Pain↓, Pain-Relieving Mechanisms of Car
*TRPV3↑, , carvacrol-induced TRPV3 activation enhances lipolysis in adipocytes via theNRF2/FSP1 a
*NRF2↑,
*Ca+2↑, TRPV3 activation in distal colon epithelial cells elevates intracellular Ca²⁺ levels and stimulates ATP release, implicating carvacrol in gut physiology and signaling
*ATP↑,
*5LO↓, s, including the inhibition of angiotensin-converting enzyme 2 (ACE2), lipoxygenase(LOX), and cyclooxygenase (COX) enzyme
*COX2/PTGS2↓,
PGE2↓, arvacrol’s anti-inflammatory effects involve theinhibition of prostaglandin E₂ (PGE₂) production via COX-2
*hepatoP↑, Carvacrol in Hepatic Protection as Natural Antioxidant
*AntiAg↑, Carvacrol has demonstrated significant antiplatelet activity, highlighting its potential therapeutic role in preventing thrombosis
*Diar↓, s essentialoil exhibited antidiarrheal effects in castor oil-induced diarrhea models, potentially mediated bymechanisms involving Kv channel activation and Ca²⁺ channel inhibition
*cardioP↑, em as promising nutraceutical candidates for alleviatingCVD-related complicat
*other↝, Carvacrol was evaluated for its therapeutic potential in managing erectile dysfunction (ED)associated with aging
*chemoPv↑, Chemopreventive Potential of Carvacrol in Detoxification pathways
*cognitive↑, carvacrol(0.5–2 mg/kg) and thymol significantly improved cognitive function in rats
*AChE↓, potent acetylcholinesterase inhibitory activity (IC₅₀: 158.94 μg/mL)
*GastroP↑, . Gastroprotective Effects of Carvacrol and Mechanism
*eff↑, . When combined with polysorbate 80 as a surfactant, carvacrol was efficiently deliveredto embryonic tissues, maintaining bioavailability during the peri-hatching phase
*BChE↓, acrol. The essential oil rich in carvacrol showedstrong inhibitory effects on AChE and butyrylcholinesterase (BChE) [
*CRP↓, d Phase II clinical trial, asthmatic patients whoreceived 1.2 mg/kg/day of carvacrol for two months showed significant improvements in pulmonaryfunction tests and a notable reduction in C-reactive protein levek

5964-

CEL,

Celecoxib pathways: pharmacokinetics and pharmacodynamics

Review,

Var,

COX2/PTGS2↓, purposefully designed as COX-2-selective inhibitors
*Pain↓, one of the most frequently prescribed drugs for the relief of pain and inflammation
*Inflam↓,
Apoptosis↑, proposed anticarcinogenic mechanisms of celecoxib include induction of apoptosis, cell cycle arrest, regulation of angiogenesis, and induction of endoplasmic reticulum (ER) stress.
TumCCA↑,
angioG↓,
ER Stress↑,
VEGF↓, Celecoxib treatment decreased the expression of vascular endothelial cell growth factor [53-55] and inhibition of matrix metalloproteinase 9
MMP9↓,
PDK1↓, inhibition of PDK1/Akt signaling correlated with celecoxib-induced apoptosis in both colon and prostate tumor cell lines [
Akt↓,
CA↓, Carbonic anhydrases (CA), enzymes that catalyze the reversible hydration of carbon dioxide, are also inhibited by celecoxib (IC50 in the low nanomolar range)
CardioT↑, selective COX-2 inhibitors, rofecoxib, valdecoxib, and celecoxib with an increased incidence of myocardial infarction, stroke, and death due to cardiovascular causes

5956-

CEL,

Direct non-cyclooxygenase-2 targets of celecoxib and their potential relevance for cancer therapy

Review,

Var,

COX2/PTGS2↓, Celecoxib (Celebrex®) was developed as a selective cyclooxygenase-2 (COX-2) inhibitor for the treatment of chronic pain.
Pain↓,
CA↓, celecoxib displayed potent CA inhibitory activity in the low nanomolar range in vitro
PDK1↓, Much excitement was generated by the finding that celecoxib could bind to and inhibit PDK1
Apoptosis↑, Celecoxib is unique among the coxibs and traditional NSAIDs, because this particular drug displays the greatest potency to induce apoptotic cell death.

6705-

DFC,

Development and Challenges of Diclofenac-Based Novel Therapeutics: Targeting Cancer and Complex Diseases

Review,

Var,

*Inflam↓, Diclofenac is a highly prescribed non-steroidal anti-inflammatory drug (NSAID) that relieves inflammation, pain, fever, and aches, used at different doses depending on clinical conditions.
*Pain↓,
*COX1↓, This drug inhibits cyclooxygenase-1 and cyclooxygenase-2 enzymes, which are responsible for the generation of prostaglandin synthesis.
*COX2/PTGS2↓,
*toxicity↝, critical challenge that appears with diclofenac and other drugs of the same class is their side effects, such as signs of stomach injuries, kidney problems, cardiovascular issues, hepatic issues, and diarrhea.
*BioAv↑, The potassium salt of diclofenac was developed to increase the rate of diclofenac absorption, which could be used in conditions where rapid pain relief is needed
*AntiAg↑, diclofenac’s inhibitory effect on platelet aggregation has also been reported
*neuroP↑, Neuroprotective Abilities of Diclofenac
ROS↑, inhibiting proliferation of cancer cells have also been reported, as shown in Figure 3, indicating its dual role. These mechanisms include inhibition of proteasomes [72], enhancement of ROS production [111], increase in p73 activity [112], and inhibi
p73↑,
Myc↓, inhibition of MYC expression and lactate transport
lactateProd↓,
TumCCA↑, Diclofenac is found to obstruct cell cycle in different cell lines, such as neural stem cells, human lymphatic endothelial cells (HLEC), osteoblasts, glioblastomas (GBM), ovarian cells, and VSMC.
PI3K↓, diclofenac-mediated apoptosis includes ROS-induced downregulation of the PI 3-kinase/Akt signaling pathway, inhibition of NF-kB activity, disturbance in proteasome activity
Akt↓,
NF-kB↓,
SOD2↓, Diclofenac impedes both expression levels and enzyme actions of SOD2
*neuroP↑, Recently, diclofenac as a curcumin adjuvant has been shown to aid anti-Alzheimer effects of curcumin in mice

6687-

DFC,

Diclofenac-containing medicines - referral

Review,

Nor,

*Pain↓, Diclofenac is a widely used medicine for relieving pain and inflammation, particularly in painful conditions such as arthritis.
*Inflam↓,
*AntiArt↑,
*cardioP↓, the overall number of heart attacks in people at moderate risk would be expected to increase by around 3 cases per year for every 1,000 people treated with diclofenac (to 11 per 1,000 people per year).

6411-

EGCG,

Pharmacological and Genetic Approaches to Downregulate FIS1 Mitigate Neuropathic Pain

in-vivo,

Nor,

*FIS1↓, As expected, EGCG treatment significantly decreased the expression of FIS1 and DRP1 in the SC-DH of SNI mice, while it had no effect on the expression of MFF
*Pain↓, downregulation of FIS1 expression within the SC-DH restored mitochondrial morphology and function, thereby exerting analgesic effects in neuropathic pain.
*ROS↓, It is noticed that EGCG, the main bioactive component of catechins, can improve mitochondria and cell function by inhibiting ROS-induced ferroptosis

6381-

Eug,

Biological Properties and Prospects for the Application of Eugenol—A Review

Review,

Var,

*eff↑, Isoeugenol derivatives have become a popular subject of research due to their fungicidal and insecticidal properties, because they exhibit greater antimicrobial activity than eugenol
*BioAv↝, Eugenol is a clear to pale yellow liquid with an oily consistency and a spicy aroma. It is sparingly soluble in water and well soluble in organic solvents.
*BioAv↝, Eugenol has low chemical stability and is sensitive to oxidation and various chemical interactions. When orally administered, it is rapidly absorbed by various organs and metabolized in the liver.
*BioAv↑, encapsulation of eugenol seems to be the best solution to prevent early absorption, improve its water solubility, and, thus, increase its activity. eugenol delivered increases at least sixfold in infected cells when delivered as solid lipid NPs
*antiOx↑, Eugenol has demonstrated various antioxidant, analgesic, antimutagenic, anti-platelet, antiallergic, anti-swelling, and anti-inflammatory properties.
*AntiAg↑,
*Inflam↓,
*AntiBio↑, It has also displayed antimicrobial effects against many human pathogens, including a wide group of Gram-positive and Gram-negative bacteria and fungi and a number of parasites
*MAOA↓, Eugenol is a popular antioxidant and monoamine oxidase (MAO) inhibitor, and it is also known to exhibit neuroprotective properties
*neuroP↑,
*ROS↓, Eugenol is known to scavenge free radicals, inhibit the generation of reactive oxygen species, prevent the production of reactive forms of nitrogen
*RNS↓,
*eff↑, The study on eugenol showed that this compound has synergistic activity with various antibiotics, such as vancomycin, penicillin, ampicillin, and erythromycin, and the combination of these compounds allowed a reduction in MIC values of 5–1000 times
NF-kB↓, killing cancer cells. The molecular mechanism is believed to include various stages: inhibiting NF-κB activation, downregulating prostaglandin synthesis, reducing cyclooxygenase-2 activity,
PGE2↓,
COX2/PTGS2↓,
TumCCA↑, inducing cell cycle arrest in the S phase, and causing apoptotic cell death by lowering inflammatory cytokine levels
Apoptosis↑,
TumCMig↓, even a low dose of eugenol interfered with the migration and invasion of carcinogenic cells, inhibited lung cancer cell viability,
TumCI↓,
tumCV↓,
PI3K↓, blocking the PI3K/Akt pathway (an intracellular signaling pathway involved in cell cycle regulation) and inhibiting MMP (matrix metalloproteinase) activity
Akt↓,
MMPs↓,
ChemoSen↑, eugenol is believed to enhance the inhibition of breast cancer stem cells by cisplatin by inhibiting the activity of aldehyde dehydrogenases (ALDH)
ALDH↓,
*Pain↓, Eugenol is a popular painkiller and anesthetic used in dental practice.
*VGSC↓, It has been found to inhibit voltage-gated sodium channels (VGSC) in the primary supply neurons of the teeth in various studies, including one based on a rat model
*IL1β↓, It is also known to be an inhibitor of pro-inflammatory mediators, including IL-1β and IL-6, tumor necrosis factor alpha (TNF-α), prostaglandin E2 (PGE2), expression of inducible oxide nitrate synthase (iNOS)
*IL6↓,
*TNF-α↓,
*iNOS↓,
*5LO↓, nuclear factor kappa B (NF-κB), and leukotriene C4 and 5-lipoxygenase (5-LOX)
*chemoPv↑, eugenol dimers have shown chemopreventive properties by inhibiting cytokine expression in macrophages

6388-

Eug,

Eugenol’s anti-cancer properties, its modulation of signalling pathways, and cascades across various cancers: A review

Review,

Var,

Dose↝, Eugenol, a significant bioactive compound, is found in cloves and other traditional Indian medicinal plants, such as cinnamon, tulsi, ginger, turmeric, and Japanese star anise, which have been reported to have significant anticancer properties.
AntiCan↑,
*Inflam↓, also exhibits different pharmacological effects (anti-inflammatory, cardio-protection, and neuroprotection).
*cardioP↑,
*neuroP↑,
angioG↓, eugenol exhibits anti-apoptotic, anti-angiogenic, and anti-metastatic properties in cancer cell lines and in vivo animal models, which we discuss in this review.
TumMeta↓,
*BioAv↑, Oral administration of eugenol promoted rapid absorption by different organs and metabolism in the liver. encapsulation is required to address the issues of early absorption, increased water solubility, and improved efficiency
*eff↑, Eugenol encapsulation as an inclusion with β-cyclodextrin, chitosan, and 2-hydroxypropyl-β-cyclodextrin nanoparticles improves its thermal stability
*toxicity↝, Eugenol at lower doses displayed minimal adverse effects, including contact dermatitis, local irritation, and rare allergic responses. However, at its higher doses, it can lead to liver and kidney damage, tissue injury, sudden onset of seizures, and
antiNeop↑, exhibit antineoplastic properties against different cancers by triggering cell cycle arrest and apoptosis in cancer cells
TumCCA↑,
Apoptosis↑,
*antiOx↑, Eugenol exhibits its antioxidant property due to its unique structural configuration, specifically the presence of an allyl group, as revealed by electron spin resonance
*lipid-P↓, Eugenol prevents lipid peroxidation (Nagababu and Lakshmaiah 1994), hexanal oxidation (Lee and Shibamoto 2001), copper-dependent LDL oxidation, and nonenzymatic peroxidation in liver mitochondria
*ROS↓, Eugenol exhibited 58–81 % DPPH radical scavenging potential in its 0.25–1.0 µM/ml concentration
*SOD↑, Eugenol protects against oxidative damage by increasing the levels of certain antioxidant enzymes, such as SOD, CAT, GST, and GPx (Huang et al. 2015).
*Catalase↑,
*GSTs↑,
*GPx↑,
*iNOS↓, Eugenol pre-treatment increased the levels of antioxidant enzymes and decreased the expression of iNOS, COX2, IL-6, and tumor necrosis factor-α (TNF-α) (Kaur et al. 2010).
*COX2/PTGS2↓,
*IL6↓,
*TNF-α↓,
*AntiArt↑, Administration of eugenol at 33 mg/kg dose in arthritis-induced male Sprague-Dawley rats decreased the swelling of paws and joints (
*Bacteria↓, Along with cinnamaldehyde and thymol, Li et al. determined eugenol's antibacterial activity against E. coli and S. aureus.
TumAuto↑, eugenol activated apoptosis and autophagy through the PI3K/AKT/FOXO3a pathway in cancer cells(breast cancer cells).
PI3K↓, PI3K/Akt/mTOR pathway inhibition
Akt↓,
FOXO3↝,
BAX↑,
mTOR↓, PI3K/Akt/mTOR pathway inhibition
NF-kB↓, NF-κB signaling pathway inhibition
P53↑, In some cancers, eugenol has been shown to upregulate p53, thereby inhibiting cancer growth.
TumCG↓,
CSCs↓, eugenol downregulated certain signaling cascades of the Wnt signaling pathway and specific cancer stem cell markers, including CD44, EpCAM, Notch1, and Oct4, in breast cancer cell lines treated with eugenol.
CD44↓,
EpCAM↓,
NOTCH1↓,
OCT4↓,
Bcl-2↓, Eugenol also downregulates the protein expressions of p85, BCL-2, PDK1, HER2, AKT, BAD, Cyclin D1, and NF-KB.
PDK1↓,
HER2/EBBR2↓,
BAD↓,
cycD1/CCND1↓,
ROS↑, EUG-medium chain triglyceride nanoemulsions Liver cancer HB8065 cells Increased the levels of ROS generation to initiated the apoptotic cell death
Casp3↑, apoptosis initiated by Caspase-3 protein upregulation
selectivity↑, Eugenol was not cytotoxic to MCF10A cells; however, it displayed cytotoxic activity in the transformed MCF10A cells (MCF10A-ras).
MMP2↓, A significant decline in matrix metalloproteinase (MMP-2, MMP-9) levels and an increase in tissue inhibitor of metalloproteinase-1 (TIMP-1) expression were also observed.
MMP9↓,
TIMP1↑,
VEGF↓, Eugenol also inhibits metastatic invasion and angiogenesis, as evident from the downregulation of MMP-2, MMP-9, VEGF, and VEGFR1, along with the upregulation of RECK and TIMP-2
VEGFR1↓,
RECK↑,
TIMP2↑,
DNAdam↑, Eugenol demonstrated an apoptosis-inducing effect in HL-60 cells, as evidenced by DNA fragmentation and a DNA ladder assay.
MMP↓, It is accompanied by a decline in mitochondrial membrane potential and thiol levels, early disruption of the lipid layer, DNA fragmentation, and activation of proapoptotic markers (Caspase-3, PARP, p53)
Thiols↓,
PARP↑,
*Pain↓, eugenol nanoemulsion may significantly reduce pain-associated arteriovenous fistula (AVF)
E2Fs↓, t interferes with several critical cancer signaling pathways, including the Wnt/b-Catenin pathway, PI3K/AKT pathway, MAPK/ERK pathway, E2F1/survivin pathway, JNK/STAT3 pathway, and NF-κB signaling pathway, among others.
survivin↓, cause E2F1/survivin downregulation, which activates apoptosis in breast cancer cells

7080-

GABA,

The Effect of Oral GABA on the Nervous System: Potential for Therapeutic Intervention

Review,

AD,

*BBB↝, While traditional beliefs questioned GABA’s ability to cross the BBB, recent research challenges this notion, proposing specific transporter systems facilitating GABA passage.
*cognitive↑, literature suggests that oral intake of GABA affects the brain illustrated by changes in EEG scans and cognitive performance, with evidence showing that GABA can have beneficial effects for multiple age groups and conditions.
*Dose↝, The gut microbiota is a source of GABA present in the gut, but oral GABA intake needs to be considered as well.
*toxicity↓, A study found that consistent administration of GABA to rats and dogs, even at doses up to 1 g/kg/day, did not exhibit any indications of toxicity
*Stress↓, Another study looked at GABA’s ability to affect brain wave patterns and reported increasing alpha and decreasing beta waves suggesting relaxation
*Inflam↓, The anti-inflammatory activity of GABA-enriched products derived from Lactobacillus fermented rice bran solution exhibited inhibitory effects on the expression of inflammatory enzymes, including inducible nitric oxide synthase and cyclooxygenase-2, a
*iNOS↓,
*COX2/PTGS2↓,
*IL6↓, and reduced the generation of pro-inflammatory cytokines like interleukin (IL)-6, IL-1β, tumor necrosis factor α, and monocyte chemoattractant protein-1
*IL1β↓,
*TNF-α↓,
*Sleep↑, GABA rice containing 26.4 mg of GABA three times daily resulted in the improvement of insomnia scores as assessed by the Kupperman Menopause Index.
*Pain↓, oral GABA supplementation or microbial-derived GABA, as a promising avenue for pain management.
*neuroP↑, potential neuroprotective properties of GABA have garnered significant interest
*eff↑, Specifically, glutamate supplementation was found to enhance memory performance by increasing acetylcholine (ACh) levels, distinguishing its effects from those of GABA
*Ach↑,
*AST↓, In support of the impact of dietary GABA on the CNS, FL50 significantly reduced AST and ALT levels induced by EtOH
*ALAT↓,
*BP↓, revealed a significant reduction in blood pressure within 2 to 4 weeks of FMG intake, and this reduction was sustained throughout the 12-week intervention period.
*other↝, Quantitative analysis of the gut microbiota composition revealed a positive correlation between the abundance of Bacteroides and GABA levels. Individuals with higher concentrations of Bacteroides exhibited elevated GABA levels in the fecal samples,

7082-

GABA,

Contributions of Gamma-Aminobutyric Acid (GABA) Produced by Lactic Acid Bacteria on Food Quality and Human Health: Current Applications and Future Prospects

Review,

AD,

*neuroP↑, possible positive effects of GABA, called a postbiotic, on neuroprotection, improving sleep quality, alleviating depression and relieving pain, the various health benefits of GABA-enriched foods such as antidiabetic, antihypertension, and anti-inflam
*Sleep↑,
*Pain↓,
*Inflam↓,
*BP↓,
*cognitive↑, GABA impacts cognitive functions such as cognition, emotion, and memory and controls central nervous system activity.
*memory↑,
*eff↑, GABA primarily exerts its influence through the brain–gut axis
*AChE↓, Research indicates that GABA derived from plant proteins such as beans, soybeans, and lentils exhibits high ACE inhibitor activity
*Wound Healing↑, GABA improved the reduction of overall healing duration and promoted early wound healing

7117-

Ge-132,

Organogermanium suppresses cell death due to oxidative stress in normal human dermal fibroblasts

in-vitro,

Nor,

*IL6↓, Furthermore, the production of IL6 induced by H2O2 was suppressed by the THGP treatment.
*Apoptosis↓, The addition of 0.59–5.9 mM THGP reduced cell death resulting from ROS damage caused by the reaction between xanthine oxidase and hypoxanthine and the direct addition of H2O2.
*toxicity↓, Repagermanium, also known as Ge-132, is a water-soluble organogermanium compound and a polymer of 3-(trihydroxygermyl) propanoic acid (THGP; (HO)3GeCH2CH2COOH), and its safety has been confirmed by several toxicological studies
Imm↑, Repagermanium has the immunostimulatory properties of inducing interferon-γ and activating natural killer cells and macrophages7,8, and these effects result in tumor suppression
IFN-γ↑,
NK cell↑,
AntiTum↑,
Pain↓, Repagermanium has also been reported to alleviate cancer pain and reduce the use of morphine as a pain killer
*Wound Healing↑, repagermanium promotes the rapid wound healing of injured skin in rats1

2521-

H2,

Oxyhydrogen Gas: A Promising Therapeutic Approach for Lung, Breast and Colorectal Cancer

Review,

CRC,

Review,

Lung,

Review,

BC,

Inflam↑, Oxyhydrogen gas, a mixture of 66% molecular hydrogen (H2) and 33% molecular oxygen (O2) has shown exceptional promise as a novel therapeutic agent due to its ability to modulate oxidative stress, inflammation, and apoptosis.
ROS↓, neutralises reactive oxygen and nitrogen species
ChemoSen↑, enhancing existing treatments and reducing harmful oxidative states in cancer cells. boosting the effectiveness of conventional therapies
p‑PI3K↓, inhibiting the PI3K/Akt phosphorylation cascade.
p‑Akt↓,
QoL↑, Similar results have been observed in breast cancer, where patients reported improved quality of life.
GutMicro↑, improves intestinal microflora dysbiosis.
chemoP↑, reduced oxidative stress and mitigated tissue damage, suggesting its potential as a cytoprotective agent in cancer patients undergoing radiation therapy or chemotherapy
radioP↑,
*NRF2↑, documented role in activating the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway.
*Catalase↑, consequently, hydrogen can enhance the expression of endogenous antioxidant enzymes, including catalase (CAT), glutathione peroxidase (GPx), haem oxygenase (e.g., HO-1), and superoxide dismutase (SOD) [45]
*GPx↑,
*HO-1↑,
*SOD↑,
*TNF-α↓, reducing the expression of proinflammatory mediators such as chemokines (e.g., CXCL15), cytokines (e.g., TNF-α), interleukins (e.g., IL-4, IL-6)
*IL4↓,
*IL6↓,
ChemoSen↑, further research demonstrates that oxyhydrogen gas enhanced the sensitivity of lung cancer cells to chemotherapy drugs, suggesting its potential as an adjuvant therapy
Appetite↑, inhaled oxyhydrogen gas over a minimum of 3 months. The results indicated substantial improvements in appetite, cognition, fatigue, pain, and sleeplessness
cognitive↑,
Pain↓,
Sleep↑,
other?, It is recommended that hydrogen should not exceed 4.6% in air or 4.1% by volume in pure oxygen gas (explosion risk)

2871-

HNK,

Antihyperalgesic Properties of Honokiol in Inflammatory Pain Models by Targeting of NF-κB and Nrf2 Signaling

in-vivo,

Nor,

honokiol 10 mg/kg i.p.

adult male BALB/c mic

*TNF-α↓, honokiol significantly reduced the expression levels of tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and vascular endothelial growth factor (VEGF).
*IL1β↓,
*IL6↓,
*VEGF↓,
*NRF2↑, honokiol was also found to potentiate the expression of nuclear factor erythroid 2–related factor 2 (Nrf2), superoxide dismutase 2 (SOD2), and heme oxygenase-1 (HO-1) levels.
*SOD2↑,
*HO-1↑,
*Inflam↓, honokiol reduced the inflammation
*Pain↓, honokiol might be a promising candidate as a new treatment for pain. results showed that honokiol remarkably reduced pain response throughout the chronic inflammatory pain model
*NO↓, Honokiol significantly reduced NO production after 6 days of treatment
toxicity↓, Treating mice with honokiol for 6 days showed no visible sign of toxicity or ill health. Obtained values, which were used as an indicator of liver and renal function, are shown in the table

7621-

HPT,

Rad,

Clinical effectiveness of combined whole body hyperthermia and external beam radiation therapy (EBRT) versus EBRT alone in patients with painful bony metastases: A phase III clinical trial study

Trial,

Pca,

Trial,

BC,

Pain↓, WBH plus RT showed significant increases in pain relief and shorter response time in comparison with RT-alone for patients with bone metastatic lesions.
Dose↝, WBH application time was 3-4 h in three fractions with at least 48-h intervals.
CR↑, Finally, the CR rate in RT + WBH revealed the most significant difference with RT-alone, 47.4% versus 5.3% respectively within 2 months post-treatment

7840-

ISQ,

Neuroprotective effects of isoquercitrin in diabetic neuropathy via Wnt/β-catenin signaling pathway inhibition

in-vivo,

Diabetic,

2-week intraperitoneal treatment of ISQ was given to diabetic rats.

*Pain↓, Treatment with ISQ, both intrathecally (10 and 30 μM) and intraperitoneally (10 mg/kg), significantly ameliorated the alterations in behavioral pain thresholds and improved functional parameters in diabetic rats
*Wnt↓, ISQ also downregulated the expression of Wnt/β-catenin pathway proteins significantly in diabetic rats as compared to vehicle-treated diabetic rats.
*β-catenin/ZEB1↓,
*neuroP↑, Results of the present study suggest the neuroprotective potential of ISQ in the treatment of DN via inhibition of Wnt/β-catenin signaling pathway.

1272-

LA,

Lactobacillus johnsonii N6.2 Modulates the Host Immune Responses: A Double-Blind, Randomized Trial in Healthy Adults

Trial,

Nor,

*Pain↓, In fact, L. johnsonii N6.2 administration significantly decreased the occurrence of abdominal pain, indigestion, and cephalic syndromes
*other↑, Moreover, an increase of circulating effector Th1 cells (CD45RO+CD183+CD196−) and cytotoxic CD8+ T cells subset was observed in the L. johnsonii N6.2 group.

6541-

MeSal,

Toxicology Answer: Oil of Wintergreen

Review,

Nor,

*Inflam↓, Commercially, and in the modern apothecary, it is used for its anti-inflammatory, antiseptic, and scent properties to treat joint, ligament, and soft tissue pain.
*Pain↓,
*BioAv↝, Ten to 20 percent of MS is absorbed through the skin after application.
*BloodF↑, produces a local vasodilatory action which increases dermal blood flow, a local rise in temperature, and a sense of warmth;
*toxicity↑, Ingestion of pure oil of Wintergreen, such as in aromatherapy products, has caused poisoning and death in children due to its high concentration of MS — up to 98 percent in some products

6939-

MF,

A prospective, randomized, placebo controlled, double-blind study of pelvic electromagnetic therapy for the treatment of chronic pelvic pain syndrome with 1 year of followup

Trial,

Nor,

 21 men with a mean age of 47.8 years

*Pain↓, pelvic floor electromagnetic therapy may be a promising new noninvasive option for chronic pelvic pain syndrome in men.

6941-

MF,

Ex,

The effects of pulsed electromagnetic field therapy on muscle strength and pain in patients with end-stage knee osteoarthritis: a randomized controlled trial

Trial,

Arthritis,

Sixty patients OA

*Strength↑, Significant improvements in symptomatic knee extension muscle strength (SKE, p = 0.001), flexion strength (SKF, p = 0.011), contralateral knee extension muscle strength (CKE, p = 0.002), and flexion strength, were observed for the PEMF
*Pain↓, combination of PEMF therapy and home-based exercise superiorly improved knee muscle strength and reduced pain in end-stage knee OA subjects
*eff↑, whereas male patients were more responsive to PEMF therapy in the form of pain relief.
*Dose↝, uniform 1mT amplitude PEMFs at a frequency of 50 Hz for a duration of 10 min per session. (figure1 looks helmholz style, or large single coil)

6940-

MF,

Meta-analysis of the effectiveness and safety of magnetic stimulation for chronic pelvic pain

Review,

BPH,

*UFR↑, Our meta-analysis revealed that extracorporeal MS significantly reduced NIH-CPSI scores [MD = -6.65; 95% CI (-8.15, -5.15), P < 0.00001] and improved Qmax [MD = 2.98; 95% CI (1.36, 4.59), P = 0.0003] compared to the control group.
*other?, MS uses magnetic fields to stimulate the central and peripheral nervous systems non-invasively, thereby enhancing the activity of enzymes that catalyze the hydrolysis of pain-inducing substances
*Pain↓, This action contributes significantly to reducing the presence of these substances, thus mitigating pain and discomfort.
*BloodF↑,
*other↑, Furthermore, positioning magnetic coils at the sacral nerve roots significantly promotes bladder emptying. MS at this location stimulates the sacral nerve, inducing muscle contractions that trigger urination
*Inflam↓, MS modulates macrophage regenerative phenotypes and enhances the synthesis of anti-inflammatory mediators, thereby mitigating inflammatory response.
*QoL↑, Specifically, all three dimensions of the questionnaire - pain symptoms, urination symptoms, and quality of life - showed marked improvement.

4349-

MF,

Long-term effect of full-body pulsed electromagnetic field and exercise protocol in the treatment of men with osteopenia or osteoporosis: A randomized placebo-controlled trial

Trial,

ostP,

0.01–15,000 Hz, with sinusoidal, rectangular, multi-resonance, impulse, or sawtooth waveforms, the full-body maximum intensity is 30 gauss (3,000 microTesla)

Ninety-five males with osteopenia or osteoporosis

*BMD↑, The BMD of total hip and lumbar spine was significantly increased post-treatment in all groups
*Pain↓, PEMFs also help patients with osteoporosis feel better by reducing pain, improving functional results and improving quality of life (QoL)
*QoL↑,
*toxicity↓, PEMF therapy has gained extensive use due to its quick effects, ease of use, and lack of side effects
*Dose↝, 30 min/day, with intensity 100%, and frequency 5-15 Hz, three times/week.
*Inflam↓, PEMFs have a considerable anti-inflammatory and analgesic effect on the joint environment (Varani et al., 2017).

505-

MF,

Amplitude-modulated electromagnetic fields for the treatment of cancer: Discovery of tumor-specific frequencies and assessment of a novel therapeutic approach

Case Report,

NA,

Pain↓, Within two weeks of experimental treatment initiation with breast cancer-specific frequencies, the patient reported complete disappearance of her pain
OS↑, two of the cases, 34mnts, and 50mnts

192-

MF,

The use of magnetic fields in treatment of patients with rheumatoid arthritis. Review of the literature

Review,

Arthritis,

 2 mT, 12 Hz

 15 to 30 minutes, and the treatments are performed 1–2 times per day for several weeks

*Dose↝, According Cieślińska-Świder [14], magnetic intensity of 2 mT and frequency of 12 Hz are used in arthritis. The recommended treatment time is from 15 to 30 minutes, and the treatments are performed 1–2 times per day for several weeks
Pain↓, . The authors showed that the magnetic field resulted in the reduction of pain in 82% of the respondents
Inflam↓, There was a decrease in swelling and reduction in the duration of morning stiffness.
Sleep↑, 64 mT decreased motor activity during sleep, which contributed to the improvement of its quality.

4111-

MF,

Coupling of pulsed electromagnetic fields (PEMF) therapy to molecular grounds of the cell

Review,

Arthritis,

*Inflam↓, ultimately lead to a dampening of inflammatory signals like interleukins
*Cartilage↑, this therapy has positive effects for the regeneration of musculoskeletal tissues such as cartilage, bone, tendon and ligament
*Pain↓, Ryang We et al. [18] found a significant beneficial effect of PEMF on WOMAC pain scores at 1 month compared with a sham treatment
*QoL↑, significant improvements in mobility, daily activity score as well as global score during treatment of acute osteoarthritis of knee joint
*Dose↝, PEMF stimulation (38 Hz, 2 mT) for 2 h per day enhanced osteoblastic functions through amelioration of the cytoskeletal organization;
*VEGF↑, increase of anti-inflammatory prostaglandins, and a huge rise in the Vascular Endothelial Growth Factor (VEGF)-A-mRNA transcription.
*NO↑, stimulatory effect of PEMF on osteoblast proliferation and differentiation is accompanied by an increase in nitric oxide (NO) synthesis
*TGF-β↑, Transforming Growth Factor (TGF-β) family is enhanced by PEMF[67] and local expression of TGF-β results in improved bone fracture healing
*MMP9↓, PEMF treatment suppressed IL-1β-mediated up-regulation of MMP-9 protein levels.
*PGE2↑, Sontag and Dertinger [97] investigated the liberation of prostaglandin E2 (PGE2) during application of EMF of different frequencies: here “windows” at 6 and 16 Hz were found, where PGE was 200% above 0 Hz baseline.
*GPx3↑, PEMF exposure also induced expression of GPX3, SOD2, CAT and GSR on mRNA, protein and enzyme activity level
*SOD2↑,
*Catalase↑,
*GSR↑,
*Ca+2↑, many EMF-effect studies is a direct action on voltage-gated calcium channels (VGCCs) (Figure 1). This is normally accompanied by a rapid increase of Ca2+

3566-

MF,

Positive and Negative Effects of Administering a Magnetic Field to Patients with Rheumatoid Arthritis (RA)

Study,

Arthritis,

39 patients with RA, who were randomly assigned to two groups: SMF—static magnetic field (n = 18) and PEMF

*Inflam↓, Magnetotherapy applied to patients with rheumatoid arthritis (RA) produces anti-inflammatory, analgesic and antioedema effects.
*QoL↑, findings show improved functional status by 0.26 points on average (p = 0.0166) measured with the Health Assessment Questionnaire (HAQ-20),
*Pain↓, reduced pain by 2.2 points on average (p = 0.0000) on the Visual Analogue Scale (VAS)
*motorD↑, decreased duration of morning stiffness by 23.2 min on average (p = 0.0010) and reduced severity of morning stiffness by 15.2 points on average. entire group showed an increase in the range of motion in the joints of the dominant hand by 1.9 mm on av
*toxicity↓, Magnetotherapy, being a non-thermal method, is safe and rarely causes negative effects
*Cartilage↑, it slows down degenerative processes in the porcine articular cartilage.
*Inflam↓, Conversely, in the PEMF group, the hand volume decreased by as much as 19.5 mm3 on average and the change was statistically significant.

3568-

MF,

The Efficacy of Pulsed Electromagnetic Fields on Pain, Stiffness, and Physical Function in Osteoarthritis: A Systematic Review and Meta-Analysis

Review,

Arthritis,

OA patients treated with PEMF

*eff↑, Compared with the control groups, the PEMF treatment yielded a more favorable output.
*Pain↓, PEMF alleviated pain (standardized mean differences [SMD] = 0.71, 95% confidence interval [CI]: 0.08–1.34, p = 0.03),
*motorD↑, improved stiffness (SMD = 1.34, 95% CI: 0.45–2.23,p=0.003), and restored physical function (SMD = 1.52, 95% CI: 0.49–2.55,p=0.004).

3569-

MF,

Current Evidence Using Pulsed Electromagnetic Fields in Osteoarthritis: A Systematic Review

Review,

Arthritis,

*Pain↓, Pain reduction, assessed through VAS and WOMAC scores, showed significant improvement (60% decrease in VAS, 42% improvement in WOMAC). The treatment duration varied (15 to 90 days), with diverse PEMF devices used
*QoL↑, Secondary outcomes included improvements in quality of life, reduced medication usage, and enhanced physical function.
*motorD↑,

224-

MFrot,

MF,

A pilot study of extremely low-frequency magnetic fields in advanced non-small cell lung cancer: Effects on survival and palliation of general symptoms

Human,

NSCLC,

 420 r/min, 0.4-T:2 h per day, 5 days per week for 6–10 weeks

 13 advanced NSCLC patients

PleEff↓,
breath↑, decreased shortness of breath
Pain↓,
Appetite↑,
Strength↑,
BowelM↑, regular Bowel Movements
OS↑, ELF-MFs may prolong survival and improve general symptoms of advanced NSCLC patients. Median survival 6 mnts vs 4mnts. median survival of patients treated with ELF-MFs was longer than that of those receiving supportive care.

198-

MFrot,

MF,

Biological effects of rotating magnetic field: A review from 1969 to 2021

Review,

Var,

AntiCan↑, RMF can inhibit the growth of various types of cancer cells in vitro and in vivo and improve clinical symptoms of patients with advanced cancer.
breath↑, 0.4T, 7Hz RMF was applied to treat 13 advanced non-small cell lung cancer patients (2 h/day, 5 days per week, for 6–10 weeks)
Pain↓, Decreased pleural effusion (2 patients, 15.4%), remission of shortness of breath (5 patients, 38.5%), relief of cancer pain (5 patients, 38.5%), increased appetite (6 patients, 46.2%), improved physical strength (9 patients, 69.2%), regular bowel mov
Appetite↑,
Strength↑,
BowelM↑,
TumMeta↓, The same RMF (2 h/day, for 43 days) can also suppress the growth and metastasis of B16-F10 cells in vivo
TumCCA↑, The up-regulated transcription of miR-34a induced cell proliferation inhibition, cell cycle arrest, and cell senescence by targeting E2F1/E2F3, two members of E2F family which are major regulators of the cell cycle,
ETC↓, 2h exposure) effectively inhibited the growth of two types of cultured brain cancer cells, glioblastoma cells and diffuse intrinsic pontine glioma cells. They found that the mitochondrial electron transport chain was significantly disturbed by RMF,
MMP↓, which caused loss of mitochondrial integrity, decreased mitochondrial carbon flux in cancer cells, and eventual cancer cell death (Sharpe et al., 2021).
TumCD↑,
selectivity↑, same group further reported that the same RMF can also selectively kill cultured human glioblastoma and non-small cell lung cancer cells, and leave normal cells unharmed
ROS↑, Mechanistic studies revealed that RMF can increase the mitochondrial ROS level, which further activated the caspase-3 and disturbed the electron fflow in the respiratory chain pathway in cancer cells. (Helekar et al., 2021).
Casp3↑,
TumCG↓, 0.4T, 7.5Hz RMF (2 h/day, for 5 days) inhibited the growth of mouse melanoma cell line B16–F10 in vitro,
TumCCA↑, and its mechanism involved cell cycle arrest and decomposition of chromatins.
ChrMod↑,
TumMeta↓, (2 h/day, for 43 days) can also suppress the growth and metastasis of B16–F10 cells in vivo,
Imm↑, benefiting from improved immune function, including decreased regulatory T cells, increased T cells, and dendritic cells
DCells↑,
Akt↓, inhibiting the activation of the AKT pathway (Tang et al., 2016). T
OS⇅, 51 women with advanced breast cancer underwent RMF treatment. The results showed that 27 patients among them achieved signicant therapeutic effects, and there were no side-effects
toxicity↓,
QoL↑, 13 advanced non-small cell lung cancer patients the quality of life was improved in different degrees. Median survival and 1-year survival rate was 50% and 100% longer
hepatoP↑, In addition, it seems that the RMF can also attenuate liver damage in mice bearing MCF7 and GIST-T1 cells (Zha et al., 2018)
Pain↓, The results showed that the RMF treatment reduced abdominal pain by 42.9% (9/21), nausea/vomiting by 19.0% (4/21), weight loss by 52.4% (11/21), ongoing blood loss by 9.5% (2/21), improved physical strength by 23.8% (5/21) and sleep quality by 19.0%
Weight↑,
Strength↑,
Sleep↑,
IL6↓, Furthermore, decreased levels of interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and keratinocyte-derived chemokine (KC) were observed
CD4+↑, it was discovered that macrophages and dendritic cells were activated, CD4+ T and CD8+ T lymphocytes increased, and the ratio of Th17/Treg was balanced.
CD8+↑,
Ca+2↑, effects of RMF were strongly associated with increased calcium tunnel activity and intracellular Ca2+ level in CNS
radioP↑, These results suggest that RMF may be helpful to alleviate the damage of hematopoietic function caused by radiotherapy and chemotherapy
chemoP↑,
*BMD↑, 0.4T, 8Hz RMF treatment (30min/day, for 30 days) along with calcium supplement, synergistically improved bone density
*AntiAge↑, In 2019, Xu et al. reported that a 4h exposure to a 0.2T, 4Hz RMF delayed the aging of human umbilical vein endothelial cells (HUVEC)
*AMPK↑, Mechanistic research revealed that RMF treatment increased the expression of AMPK while reducing the expression of p21, p53 and mTOR.
*P21↓,
*P53↓,
*mTOR↓,
*OS↑, They also discovered that the RMF (2 h/day, for 6, 10 or 14days) can prolong the health status lifespan of Caenorhabditis elegans.
*β-Endo↑, 0.1–0.8T, 0.33Hz RMF treatment signicantly increased the β-endorphin level in the blood of rabbits and humans (23 times higher than before). Moreover, it decreased serotonin (5-HT) in brains, small intestine tissue and serum of mice.
*5HT↓,

217-

MFrot,

MF,

Effect of low-frequency rotary magnetic fields on advanced gastric cancer

in-vivo,

GC,

HL-60

 420 r/min, 0.4-T

in-vivo,

GC,

SK-HEP-1

OS↑, 8months compared to 3-5 normally
Pain↓, low-frequency rotary MFs improved abdominal pain in 9/21 (42.9%), nausea/vomiting in 4/21 (19.0%), weight loss in 11/21 (52.4%), ongoing blood loss in 2/21 (9.5%), physical strength in 5/21 (23.8%), and sleep quality in 4/21 (19.0%) patients.
ChemoSideEff↓,
Weight↑,
Strength↑,
Sleep↑,

Showing Research Papers: 1 to 50 of 64
Page 1 of 2 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 64

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 1,
Total Targets: 172

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AntiArt↑, 2, AntiBio↑, 3, Stress↓, 1, UFR↑, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 8, Catalase↑, 7, GPx↑, 4, GPx3↑, 1, GSH↑, 2, GSR↑, 2, GSTs↑, 1, HO-1↑, 2, Keap1↑, 1, lipid-P↓, 3, MDA↓, 3, NRF2↑, 5, PARK2↑, 1, RNS↓, 1, ROS↓, 7, ROS↑, 1, SIRT3↑, 1, SOD↑, 6, SOD2↑, 2, TBARS↓, 1, uricA↓, 1,

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 2, FIS1↓, 1, Insulin↑, 1, MMP↓, 1, MMP↑, 1, PINK1↑, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1, AMPK↑, 2, glucose↓, 1, LDH↓, 1,

Cell Death(tgid=5) ⓘ

Apoptosis↓, 2, BAX↓, 1, Bcl-2↑, 1, Casp3↓, 1, Cyt‑c↓, 1, iNOS↓, 5, necrosis↓, 1, TRPV1↑, 3,

Kinase & Signal Transduction(tgid=6) ⓘ

TRPV3↑, 1,

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 1, other?, 1, other↑, 3, other↝, 2, TFAM↑, 1,

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1, LC3B↑, 1, p62↓, 1,

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,

Cell Cycle & Senescence(tgid=11) ⓘ

P21↓, 1,

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

mTOR↓, 1, TRPM7↓, 1, VGSC↓, 1, Wnt↓, 1,

Migration(tgid=13) ⓘ

5LO↓, 2, AntiAg↑, 7, Ca+2↑, 2, Cartilage↑, 2, MMP13↓, 1, MMP9↓, 1, TGF-β↑, 1, β-catenin/ZEB1↓, 1, β-Endo↑, 1,

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1, NO↑, 1, VEGF↓, 1, VEGF↑, 1,

Barriers & Transport(tgid=15) ⓘ

BBB↑, 2, BBB↝, 1, GastroP↑, 2,

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1, COX1↓, 1, COX2/PTGS2↓, 9, CRP↓, 1, IL1β↓, 5, IL4↓, 1, IL6↓, 7, IL6↑, 1, Imm↑, 2, Inflam↓, 20, NF-kB↓, 2, PGE2↑, 1, TNF-α↓, 8,

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 1, AChE↓, 3, BChE↓, 2, MAOA↓, 1, tau↓, 1,

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 2, BACE/β-secretase↓, 1, NLRP3↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1, BioAv↑, 8, BioAv↝, 3, BioEnh↑, 1, Dose↝, 6, eff↑, 10,

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1, AST↓, 2, BloodF↑, 3, BMD↑, 2, BP↓, 3, creat↓, 1, CRP↓, 1, IL6↓, 7, IL6↑, 1, LDH↓, 1,

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1, AntiCan↑, 2, AntiDiabetic↑, 2, cardioP↓, 1, cardioP↑, 7, chemoPv↑, 2, cognitive↑, 4, hepatoP↑, 3, memory↑, 2, motorD↓, 1, motorD↑, 5, neuroP↑, 12, NP/CIPN↓, 1, Obesity↓, 2, OS↑, 2, Pain↓, 31, QoL↑, 5, RenoP↑, 2, Risk↓, 2, Sleep↑, 2, Strength↑, 1, toxicity↓, 7, toxicity↑, 1, toxicity↝, 2, Weight↓, 1, Wound Healing↑, 3,

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1, Bacteria↓, 4, CD8+↑, 1, Diar↓, 2,
Total Targets: 141

Scientific Paper Hit Count for: Pain, Pain

13 Magnetic Fields
8 Capsaicin
3 Beta-Caryophyllene
3 Radiotherapy/Radiation
3 Carvacrol
3 Magnetic Field Rotating
2 Celecoxib
2 Diclofenac
2 Eugenol
2 Gamma-aminobutyric acid
2 Exercise
2 Methylsulfonylmethane
2 Peppermint
2 Quercetin
2 Selenite (Sodium)
1 Acetyl-l-carnitine
1 Astaxanthin
1 Aloe anthraquinones
1 Cannabidiol
1 Bromelain
1 borneol
1 α-Bisabolol / Chamomile oil
1 Butyrate
1 EGCG (Epigallocatechin Gallate)
1 Germanium Organic/Ge-132 / propagermanium (organogermanium)
1 Hydrogen Gas
1 Honokiol
1 Hyperthermia
1 isoquercitrin
1 Lactobacillus
1 Methyl salicylate / Sweet Birch oil
1 Oleuropein
1 Propolis -bee glue
1 Selenium
1 Chemotherapy
1 Turmerones
1 Vitamin C (Ascorbic Acid)
1 Whole Body Vibration

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:576  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

Pain Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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