Pain Cancer Research Results

Pain, Pain: Click to Expand ⟱

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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↓,

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↓, 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.

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↓, 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↓,
*MDA↓,

5926-

CAR,

An Updated Review of Research into Carvacrol and Its Biological Activities

Review,

Nor,

Review,

AD,

Review,

asthmatic,

*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↓,
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↓, 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↓, 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.

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

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.

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↑,

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.

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).

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↑,

3847-

MSM,

Methylsulfonylmethane: Applications and Safety of a Novel Dietary Supplement

Review,

Arthritis,

*Inflam↓, common use as an anti-inflammatory agent
*Pain↓, A variety of health-specific outcome measures are improved with MSM supplementation, including inflammation, joint/muscle pain, oxidative stress, and antioxidant capacity.
*ROS↓,
*antiOx↑,
*Dose↝, MSM is well-tolerated by most individuals at dosages of up to four grams daily, with few known and mild side effects
*Half-Life↝, Pharmacokinetic studies indicate that MSM is rapidly absorbed in rats [63,64] and humans [65], taking 2.1 h and <1 h, respectively.
*NF-kB↓, The inhibitory effect of MSM on NF-κB results in the downregulation of mRNA for interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α) in vitro
*IL1↓,
*IL6↓,
*TNF-α↓,
*iNOS↓, MSM can also diminish the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) through suppression of NF-κB;
*COX2↓,
*NLRP3↓, MSM negatively affects the expression of the NLRP3 inflammasome by downregulating the NF-κB production of the NLRP3 inflammasome transcript and/or by blocking the activation signal in the form of mitochondrial generated reactive oxygen species (ROS)
*NRF2↑, MSM influences the activation of at least four types of transcription factors: NF-κB, signal transducers and activators of transcription (STAT), p53, and nuclear factor (erythroid-derived 2)-like 2 (Nrf2).
*STAT↓, MSM has been shown to repress the expression or activities of STAT transcription factors in a number of cancer cell lines in vitro
*Cartilage↑, , in vitro studies suggest that MSM protects cartilage through its suppressive effects on IL-1β and TNF-α
*eff↑, Supplementation with glucosamine, chondroitin sulfate, MSM, guava leaf extract, and Vitamin D improved physical function in patients with knee osteoarthritis based on the Japanese Knee OA Measure
*eff↑, MSM in combination with boswellic acid was also shown to improve knee joint function as assessed through the Lequesne Index
*GSH↑, MSM is able to restore the reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio to normal levels, decrease NO production, and reduce neuronal ROS production following HIV-1 Tat exposure
*uricA↓, Humans studies show promise for MSM as an antioxidant with similar results noted, including reductions in MDA [19,167,168], protein carbonyls (PC) [167,168], and uric acid [168] and increases in GSH [167] and TEAC [159,161,168].
tumCV↓, MSM independently has been shown to be cytotoxic to cancer cells by inhibiting cell viability through the induction of cell cycle arrest [119,122,123], necrosis [119], or apoptosis
TumCCA↑,
necrosis↑,
Apoptosis↑,
VEGF↓, reduced expression of oncogenic proteins such as vascular endothelial growth factor (VEGF) [99,100,101,123], heat shock protein (HSP)90α [100], and insulin-like growth factor-1 receptor (IGF-1R)
HSP90↓,
IGF-1?,

3851-

MSM,

Efficacy of methylsulfonylmethane (MSM) in osteoarthritis pain of the knee: a pilot clinical trial

Trial,

Arthritis,

3g twice a day

*Pain↓, MSM produced significant decreases in WOMAC pain and physical function impairment
*QoL↑, MSM also produced improvement in performing activities of daily living when compared to placebo on the SF-36 evaluation

5937-

Peppermint and the gut

Review,

IBD,

other↝, The spasmolytic effect of peppermint oilhas been demonstrated on the smoothmuscle of the digestive tract in humans
*Bacteria↓, In vitro, peppermint oil possesses anti-bacterial activity on numerous bacteria including Helicobacter pylori, Escherichia coli, Salmonella enteritis and Shigella sonnei.
*Pain↓, peppermint oil capsules decreased abdominal pain by 79%
*BowelM↑, Furthermore, 83% had a more regular bowel habit

5936-

The impact of peppermint oil on the irritable bowel syndrome: a meta-analysis of the pooled clinical data

Review,

IBD,

*Pain↓, PO was shown to be a safe and effective therapy for pain and global symptoms in adults with IBS.
*other↝, PO contains L-menthol, which blocks calcium channels in smooth muscle, thus producing antispasmodic effects on the gastrointestinal tract
*Bacteria↓, PO possesses antimicrobial, anti-inflammatory, antioxidant, immunomodulating, and anesthetic activities, all of which may be relevant for the treatment of IBS
*Inflam↓,
*Imm↑,
*eff↑, specialized enteric-coating utilized in their trial consisted of a solid-state matrix that was triple-coated and designed to deliver PO with sustained release to the small intestine with fewer potential adverse effects.
*toxicity↓, Enteric-coated peppermint oil is a safe and effective therapy for the relief of abdominal pain and global symptoms and in adults with IBS.

3249-

PBG,

Can Propolis Be a Useful Adjuvant in Brain and Neurological Disorders and Injuries? A Systematic Scoping Review of the Latest Experimental Evidence

Review,

Var,

*Inflam↓, ropolis was consistently demonstrated to reduce the expression of inflammatory and oxidative markers such as malonaldehyde (MDA), tumor necrosis factor-α (TNF-α), nitric oxide (NO), and inducible nitric oxide synthase (iNOS)
*ROS↓,
*MDA↓,
*TNF-α↓,
*NO↓,
*iNOS↓,
*SOD↑, while increasing and maintaining antioxidant parameters, namely superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH)
*GPx↑,
*GSR↓,
*GSH↑,
*neuroP↑, neuroprotective effect of propolis was also demonstrated in terms of alleviating symptoms associated with aneurysm, ischemia, ischemia-reperfusion and traumatic brain injuries.
*IL6↓, Propolis reduced the expression of interleukin-6 (IL-6), TNF-α, matrix metalloproteinase-2 (MMP-2), MMP-9, monocyte chemotactic protein-1 (MCP-1), and iNOS
*MMP2↓,
*MMP9↓,
*MCP1↓,
*HSP70/HSPA5↑, while increasing the expression of protective proteins such as heat shock protein-70 (hsp70)
*motorD↑, significantly ameliorate the impairment of sensory–motor and other physical indices in animals subjected to these injuries
*Pain↓, Unsurprisingly, propolis was shown to be effective in attenuating symptoms of neuroinflammation, pain, and oxidative stress.
*VCAM-1↓, consistently shown to reduce inflammation markers such as vascular cell adhesion molecule-1 (VCAM-1), nuclear factor kappa B (NF-kB), mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK)-
*NF-kB↓,
*MAPK↓,
*JNK↓,
*IL1β↓, It also reduced the expression of reactive oxygen species (ROS) and pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α
*AChE↓, propolis inhibited the activity of both acetylcholinesterase and butyrylcholinesterase in a dose-dependent manner
*toxicity∅, Kalia et al. (2014) observed no cytotoxicity in organs, including the brain of normal mice fed up to 1000 mg propolis extract/ kg body weight.
cognitive↑, figure 4

3606-

QC,

The Effect of Quercetin on Inflammatory Factors and Clinical Symptoms in Women with Rheumatoid Arthritis: A Double-Blind, Randomized Controlled Trial

Trial,

Arthritis,

500 mg/day

50 women with RA

*motorD↑, Quercetin supplementation for 8 weeks significantly reduced EMS, morning pain, and after-activity pain
*Pain↓,
*TNF-α↓, Plasma hs-TNFα level was significantly reduced in the quercetin group compared to placebo
*IL8↓, Other studies showed that 30 mM quercetin decreased gene expression and production of IL-8, 1L-6, IL-1b, and TNFa, which are the major inflammatory cytokines i
*IL6↓,
*IL1β↓,
*NF-kB↓, also inhibited the activity of NF-kB and P38-kinase protein
*p38↓,

3343-

QC,

Quercetin, a Flavonoid with Great Pharmacological Capacity

Review,

Var,

Review,

AD,

Review,

Arthritis,

*antiOx↑, Quercetin has a potent antioxidant capacity, being able to capture reactive oxygen species (ROS), reactive nitrogen species (RNS), and reactive chlorine species (ROC),which act as reducing agents by chelating transition-metal ions.
*ROS↓, Quercetin is a potent scavenger of reactive oxygen species (ROS), protecting the organism against oxidative stress
*angioG↓,
*Inflam↓, anti-inflammatory properties; the ability to protect low-density lipoprotein (LDL) oxidation, and the ability to inhibit angiogenesis;
*BioAv↓, It is known that the bioavailability of quercetin is usually relatively low (0.17–7 μg/mL), less than 10% of what is consumed, due to its poor water solubility (hydrophobicity), chemical stability, and absorption profile.
*Half-Life↑, their slow elimination since their half-life ranges from 11 to 48 h, which could favor their accumulation in plasma after repeated intakes
*GSH↑, Animal and cell studies have demonstrated that quercetin induces the synthesis of GSH
*SOD↑, increase in the expression of superoxide dismutase (SOD), catalase (CAT), and GSH with quercetin pretreatment
*Catalase↑,
*Nrf1↑, quercetin accomplishes this process involves increasing the activity of the nuclear factor erythroid 2-related factor 2 (NRF2), enhancing its binding to the ARE, reducing its degradation
*BP↓, quercetin has been shown to inhibit ACE activity, reducing blood pressure
*cardioP↑, quercetin has positive effects on cardiovascular diseases
*IL10↓, Under the influence of quercetin, the levels of interleukin 10 (IL-10), IL-1β, and TNF-α were reduced.
*TNF-α↓,
*Aβ↓, quercetin’s ability to modulate the enzyme activity in clearing amyloid-beta (Aβ) plaques, a hallmark of AD pathology.
*GSK‐3β↓, quercetin can inhibit the activity of glycogen synthase kinase 3β,
*tau↓, thus reducing tau aggregation and neurofibrillary tangles in the brain
*neuroP↑,
*Pain↓, quercetin reduces pain and inflammation associated with arthritis
*COX2↓, quercetin included the inhibition of oxidative stress, production of cytokines such as cyclooxygenase-2 (COX-2) and proteoglycan degradation, and activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) (Nrf2/HO-1)
*NRF2↑,
*HO-1↑,
*IL1β↓, Mechanisms included decreased levels of TNF-α, IL-1β, IL-17, and monocyte chemoattractant protein-1 (MCP-1)
*IL17↓,
*MCP1↓,
PKCδ↓, studies with human leukemia 60 (HL-60) cells report that concentrations between 20 and 30 µM are sufficient to exert an inhibitory effect on cytosolic PKC activity and membrane tyrosine protein kinase (TPK) activity.
ERK↓, 50 µM resulted in the blockade of the extracellular signal-regulated kinases (ERK1/2) pathway
BAX↓, higher doses (75–100 µM) were used, as these doses reduced the expression of proapoptotic factors such as Bcl-2-associated X protein (Bax) and caspases 3 and 9
cMyc↓, induce apoptosis at concentrations of 80 µM and also causes a downregulation of cellular myelocytomatosis (c-myc) and Kirsten RAt sarcoma (K-ras) oncogenes
KRAS↓,
ROS↓, compound’s antioxidative effect changes entirely to a prooxidant effect at high concentrations, which induces selective cytotoxicity
selectivity↑, On the other hand, when noncancerous cells are exposed to quercetin, it exerts cytoprotective effects;
tumCV↓, decrease cell viability in human glioma cultures of the U-118 MG cell line as well as an increase in death by apoptosis and cell arrest at the G2 checkpoint of the cell cycle.
Apoptosis↑,
TumCCA↑,
eff↑, quercetin combined with doxorubicin can induce multinucleation of invasive tumor cells, downregulate P-glycoprotein (P-gp) expression, increase cell sensitivity to doxorubicin,
P-gp↓,
eff↑, resveratrol, quercetin, and catechin can effectively block the cell cycle and reduce cell proliferation in vivo
eff↑, cotreatment with epigallocatechin gallate (EGCG) inhibited catechol-O-methyltransferase (COMT) activity, decreasing COMT protein content and thereby arresting the cell cycle of PC-3 human prostate cancer cells
eff↑, synergistic treatment of tamoxifen and quercetin was also able to inhibit prostate tumor formation by regulating angiogenesis
eff↑, coadministration of 2.5 μM of EGCG, genistein, and quercetin suppressed the cell proliferation of a prostate cancer cell line (CWR22Rv1) by controlling androgen receptor and NAD (P)H: quinone oxidoreductase 1 (NQO1) expression
CycB/CCNB1↓, It can also downregulate cyclin B1 and cyclin-dependent kinase-1 (CDK-1),
CDK1↓,
CDK4↓, quercetin causes a decrease in cyclins D1/Cdk4 and E/Cdk2 and an increase in p21 in vascular smooth muscle cells
CDK2↓,
TOP2↓, quercetin is known to be a potent inhibitor of topoisomerase II (TopoII), a cell cycle-associated enzyme necessary for DNA replication
Cyt‑c↑, quercetin can induce apoptosis (cell death) through caspase-3 and caspase-9 activation, cytochrome c release, and poly ADP ribose polymerase (PARP) cleavage
cl‑PARP↑,
MMP↓, quercetin induces the loss of mitochondrial membrane potential, leading to the activation of the caspase cascade and cleavage of PARP.
HSP70/HSPA5↓, apoptotic effects of quercetin may result from the inhibition of HSP kinases, followed by the downregulation of HSP-70 and HSP-90 protein expression
HSP90↓,
MDM2↓, (MDM2), an onco-protein that promotes p53 destruction, can be inhibited by quercetin
RAS↓, quercetin can prevent Ras proteins from being expressed. In one study, quercetin was found to inhibit the expression of Harvey rat sarcoma (H-Ras), K-Ras, and neuroblastoma rat sarcoma (N-Ras) in human breast cancer cells,
eff↑, there was a substantial difference in EMT markers such as vimentin, N-cadherin, Snail, Slug, Twist, and E-cadherin protein expression in response to AuNPs-Qu-5, inhibiting the migration and invasion of MCF-7 and MDA-MB cells

4754-

Se,

Chemo,

The effect of selenium yeast in the prevention of adverse reactions related to platinum-based combination therapy in patients with malignant tumors

Trial,

Var,

selenium yeast at a dose of 200 ug daily

 86 patients with malignant tumors treate

chemoP↑, Patients with selenium yeast treatment after chemotherapy had better appetites and more stable body weights than those without selenium yeast
QoL↑, quality of life of the patients, as evidenced by the elevated Karnofsky Performance Status (KPS) scores of the two groups, and selenium yeast treatment potentiated this improvement
chemoP↑, Selenium yeast treatment significantly reduced the incidence of adverse reactions in patients after chemotherapy by 23.26% (p<0.05), and patients also experienced milder adverse reactions after selenium yeast administration
Pain↓, Chemotherapy with selenium yeast treatment provided better pain mitigation for patients vs. without selenium yeast administration

4742-

SSE,

Antitumor Effects of Selenium

Review,

Var,

Review,

Arthritis,

Review,

Sepsis,

*antiOx↓, Functions of selenium are diverse as antioxidant, anti-inflammation, increased immunity, reduced cancer incidence, blocking tumor invasion and metastasis, and further clinical application as treatment with radiation and chemotherapy.
*Inflam↓,
Risk↓,
TumCI↓,
TumMeta↓,
radioP↑,
chemoP↑,
Apoptosis↑, (SeDG), which induces cytotoxicity as cell apoptosis, ROS production, DNA damage, and adenosine-methionine methylation in the cellular nucleus
ROS↑,
DNAdam↑,
Dose↑, In our study, advanced cancer patients can tolerate until 5000 μg of sodium selenite in combination with radiation and chemotherapy since the half-life of sodium selenite may be relatively short
selectivity↑, selenium may accumulates more in cancer cells than that of normal cells, which may be toxic to the cancer cells.
*other↓, Se-methylselenocysteine (MSeC) is most abundant in garlic, broccoli, walnut, and some other plant products.
*BioAv↑, Most Se compounds are readily absorbed from the diet and are mainly metabolized in the liver.
ROS↑, Methylselenol induced apoptosis by ROS production, subsequently altered mitochondrial membrane potential, and, further, induced caspases’ activity.
MMP↓,
Casp↑,
*Imm↑, Se activates immune functions via the activation of IL-2 receptor [59].
*Pain↓, Supplementation with 200 μg Se in a group of rheumatoid arthritis patients for three months significantly reduced pain and joint involvement
Sepsis↓, Se plays an important role in defense against acute illness, such as sepsis syndrome
MMP2↓, Several experiments by our group demonstrate that selenite inhibits tumor invasion by blocking MMP-2 and -9 expression
MMP9↓,
*Half-Life↓, a short half-life of sodium selenite and more accumulation of the Se in the cancer cells may be more toxic in cancer cells than that in normal cells.

5078-

SSE,

Rad,

Results from a Phase 1 Study of Sodium Selenite in Combination with Palliative Radiation Therapy in Patients with Metastatic Cancer

Trial,

Pca,

33 mg dose level,

15 patients with metastatic cancer treated with selenite (5.5 to 49.5 mg) orally as a single dose 2 hours before each radiation therapy (RT) treatment.

Half-Life↝, The half-life of selenite was 18.5 hours.
OS↑, Most patients had stabilization of disease within the RT fields, with some demonstrating objective evidence of tumor regression.
Pain↓, Most patients had a marked improvement in pain and seven out of nine patients with prostate cancer had a decrease in PSA ranging from 11–78%.
PSA↓,
GSH↓, selenite depletes cells of an important antioxidant, glutathione (GSH), and results in the generation of superoxide, a highly reactive and toxic radical that results in the generation of reactive oxygen species (ROS).
ROS↑,
selectivity↑, 1) prostate cancer cells are more sensitive to selenium (sodium selenite)-induced apoptosis than normal prostate epithelial cells
TumCG↓, 2) Selenite induces significant growth inhibition of well-established prostate cancer tumors in mice at doses that have no detectable toxicity when administered both ip and po, a
AR↓, 3) Selenite disrupts androgen receptor (AR) signaling, with inhibition of AR expression
Dose↑, This simulation reveals that only the higher dose levels (33 mg and 49.5 mg) reach the desired therapeutic range after a single dose.
ChemoSen↑, In another study of selenite (0.2 mg/kg per day for 7 days) in combination with chemotherapy, addition of selenite resulted in a significant increase in the percentage of apoptotic lymphoma cells and clinical response compared to patients treated wit
RadioS↑, sodium selenite was studied in 15 patients with advanced/metastatic tumors receiving concurrent sodium selenite with palliative radiation therapy.

625-

VitC,

The Effect of Vitamin C (Ascorbic Acid) in the Treatment of Patients with Cancer: A Systematic Review

OS↑, In 7 studies, the researchers found a positive effect of vitamin C on survival time
Pain↓, 15 patients with bone metastasis IVC had a positive effect on relief of pain

1753-

WBV,

Ex,

Physical Exercise with or without Whole-Body Vibration in Breast Cancer Patients Suffering from Aromatase Inhibitor—Induced Musculoskeletal Symptoms: A Pilot Randomized Clinical Study

Trial,

BC,

Pain↓, The WBV group (mean age: 51.73 ± 10.73 years; body mass index (BMI): 25.56 ± 5.17 kg/m2) showed a statistically significant pain reduction
Strength↑, Concurrently, muscle strength, physical performance, and quality of life significantly improved in both groups, without significant differences between groups
QoL↑,
Dose∅, with a frequency of 30 Hz, peak-to-peak amplitude of 1.15 mm. in squatting position (110° knee flexion)

Showing Research Papers: 1 to 44 of 44

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 44

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

CD8+↑, 1, Sepsis↓, 1,
Total Targets: 145

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↓, 1, antiOx↑, 5, Catalase↑, 5, GPx↑, 4, GPx3↑, 1, GSH↑, 3, GSR↓, 1, GSR↑, 2, HO-1↑, 3, lipid-P↓, 1, MDA↓, 3, Nrf1↑, 1, NRF2↑, 5, ROS↓, 5, SOD↑, 5, SOD2↑, 2, uricA↓, 1,

Mitochondria & Bioenergetics ⓘ

ATP↑, 1, Insulin↑, 1,

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1, glucose↓, 1, LDH↓, 1,

Cell Death ⓘ

iNOS↓, 2, JNK↓, 1, MAPK↓, 1, necrosis↓, 1, p38↓, 1, TRPV1↑, 3,

Kinase & Signal Transduction ⓘ

TRPV3↑, 1,

Transcription & Epigenetics ⓘ

BowelM↑, 1, other↓, 1, other↑, 2, other↝, 2,

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,

DNA Damage & Repair ⓘ

P53↓, 1,

Cell Cycle & Senescence ⓘ

P21↓, 1,

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1, mTOR↓, 1, STAT↓, 1, TRPM7↓, 1,

Migration ⓘ

5LO↓, 1, AntiAg↑, 5, Ca+2↑, 2, Cartilage↑, 3, MMP2↓, 1, MMP9↓, 2, TGF-β↑, 1, VCAM-1↓, 1, β-Endo↑, 1,

Angiogenesis & Vasculature ⓘ

angioG↓, 1, NO↓, 2, NO↑, 1, VEGF↓, 1, VEGF↑, 1,

Barriers & Transport ⓘ

GastroP↑, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 5, CRP↓, 1, IL1↓, 1, IL10↓, 1, IL17↓, 1, IL1β↓, 5, IL4↓, 1, IL6↓, 5, IL8↓, 1, Imm↑, 3, Inflam↓, 15, MCP1↓, 2, NF-kB↓, 4, PGE2↑, 1, TNF-α↓, 7,

Synaptic & Neurotransmission ⓘ

5HT↓, 1, AChE↓, 2, BChE↓, 1, tau↓, 2,

Protein Aggregation ⓘ

Aβ↓, 2, NLRP3↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 2, BioAv↑, 3, Dose↝, 5, eff↑, 6, Half-Life↓, 1, Half-Life↑, 1, Half-Life↝, 1,

Clinical Biomarkers ⓘ

AST↓, 1, BMD↑, 2, BP↓, 2, CRP↓, 1, IL6↓, 5, LDH↓, 1,

Functional Outcomes ⓘ

AntiAge↑, 1, AntiCan↑, 2, AntiDiabetic↑, 2, cardioP↑, 5, chemoPv↑, 1, cognitive↑, 2, hepatoP↑, 3, memory↑, 1, motorD↓, 1, motorD↑, 6, neuroP↑, 6, Obesity↓, 2, OS↑, 2, Pain↓, 24, QoL↑, 5, RenoP↑, 1, Risk↓, 2, toxicity↓, 5, toxicity∅, 1, Weight↓, 1, Wound Healing↑, 1,

Infection & Microbiome ⓘ

Bacteria↓, 5, Diar↓, 2,
Total Targets: 112

Scientific Paper Hit Count for: Pain, Pain

10 Magnetic Fields
8 Capsaicin
3 Carvacrol
3 Magnetic Field Rotating
2 Radiotherapy/Radiation
2 Celecoxib
2 Methylsulfonylmethane
2 Peppermint
2 Quercetin
2 Selenite (Sodium)
1 Acetyl-l-carnitine
1 Astaxanthin
1 Aloe anthraquinones
1 Bromelain
1 borneol
1 Butyrate
1 Hydrogen Gas
1 Honokiol
1 Lactobacillus
1 Propolis -bee glue
1 Selenium
1 Chemotherapy
1 Vitamin C (Ascorbic Acid)
1 Whole Body Vibration
1 Exercise

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:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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