GutMicro Cancer Research Results

GutMicro, Gut Microbiota: Click to Expand ⟱

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Gut microbiome may affect responses to numerous forms of cancer therapy.
The gut microbiota plays a multifaceted role in cancer biology, influencing tumor development, progression, and patient prognosis. Dysbiosis and specific microbial populations have been linked to various cancers, with implications for patient outcomes. While the relationship between gut microbiota and cancer prognosis is an active area of research, it holds promise for the development of microbiome-based biomarkers and therapeutic strategies in oncology.

Scientific Papers found: Click to Expand⟱

3538-

5-HTP,

Oral Administration of 5-Hydroxytryptophan Restores Gut Microbiota Dysbiosis in a Mouse Model of Depression

in-vivo,

Nor,

mice

*GutMicro↑, The diversity and richness of gut microbial communities and relative abundance of specific microbial taxa at both phylum and genus levels were partially recovered.
*BBB↑, 5-HTP, a precursor of 5-HT, can easily cross the blood-brain barrier without requiring a transporter and increase the brain 5-HT levels to yield an antidepressant-like effect
*5HT↑, capacity to increase the brain and gastrointestinal tract 5-HT levels after oral administration
*Weight↓, 5-HTP could reduce the body weights of both healthy mice and mice with depression-like behaviors.

1161-

ACNs,

immuno,

Bilberry anthocyanin extracts enhance anti-PD-L1 efficiency by modulating gut microbiota

in-vivo,

Colon,

MC38

mouse

GutMicro↑, increase in the fecal abundance of Clostridia and Lactobacillus johnsonii and improved effective community diversity.

3972-

ACNs,

Recent Research on the Health Benefits of Blueberries and Their Anthocyanins

Review,

AD,

Review,

Park,

*cardioP↑, Epidemiological studies associate regular, moderate intake of blueberries and/or anthocyanins with reduced risk of cardiovascular disease, death, and type 2 diabetes, and with improved weight maintenance and neuroprotection.
*neuroP↑,
*Inflam↓, Among the more important healthful aspects of blueberries are their anti-inflammatory and antioxidant actions and their beneficial effects on vascular and glucoregulatory function
*antiOx↓,
*GutMicro↑, Blueberry phytochemicals may affect gastrointestinal microflora and contribute to host health
*Half-Life↑, However, >50% of the 13C still remained in the body after 48 h
*LDL↓, controlled study of 58 diabetic patients, blueberry intake led to a decline in LDL cholesterol, triglycerides, and adiponectin and an increase in HDL cholesterol
*adiP↓,
*HDL↑,
*CRP↓, reduction was documented in inflammatory markers, including serum high-sensitivity C-reactive protein, soluble vascular adhesion molecule-1, and plasma IL-1β
*IL1β↓,
*Risk↓, lower Parkinson disease risk was associated with the highest quintile of anthocyanin (RR: 0.76) and berry (RR: 0.77) intake
*Risk↓, Nurse's Health Study, greater intake of blueberries and strawberries was associated with slower rates of cognitive decline in older adults, with an estimated delay in decline of about 2.5 y
*cognitive↑, Cognitive performance in elderly adults improved after 12 wk of daily intake of blueberry (94) or Concord grape (95) juice.
*memory↑, Better task switching and reduced interference in memory was found in healthy older adults after 90 d of blueberry supplementation
*other↑, After 12 wk of blueberry consumption, greater brain activity was detected using magnetic resonance imaging in healthy older adults during a cognitive challenge.
*BOLD↑, Similarly, during a memory test, regional blood oxygen level-dependent activity detected by MRI (99) was enhanced in the subjects taking blueberry, but not in those taking placebo.
*NO↓, 50–200 mg/d bilberry showed a dose-dependent decrease in neurotoxic NO and malondialdehyde, combined with an increase in neuroprotective antioxidant capacity due to glutathione, vitamin C, superoxide dismutase, and glutathione peroxidase
*MDA↓,
*GSH↑,
*VitC↑,
*SOD↑,
*GPx↑,
*eff↓, The percentage loss of blueberry anthocyanins during −18°C storage was 12% after 10 mo of storage
*eff↓, Freeze-dried blueberry powder loses anthocyanins in a temperature-dependent manner with a half-life of 139, 39, and 12 d when stored at 25, 42, and 60°C, respectively
*eff↓, Blueberries are low in ascorbic acid and high in anthocyanins (187), and notably anthocyanins are readily degraded by ascorbic acid
*eff↝, Shelf-stable blueberry products like jam (196), juice (197), and extracts (198) can lose polyphenolic compounds when stored at ambient temperature whereas refrigeration mitigates losses.
*Risk↓, It can be safely stated that daily moderate intake (50 mg anthocyanins, one-third cup of blueberries) can mitigate the risk of diseases and conditions of major socioeconomic importance in the Western world.

540-

Akk,

Akkermansia muciniphila: a potential booster to improve the effectiveness of cancer immunotherapy

Analysis,

NA,

GutMicro↑,
carcinogenesis↓,
ChemoSideEff↓,

541-

Akk,

Akkermansia muciniphila as a Next-Generation Probiotic in Modulating Human Metabolic Homeostasis and Disease Progression: A Role Mediated by Gut-Liver-Brain Axes?

Review,

NA,

GutMicro↑,
PD-1↝,
CD8+↑, CD8+ cytotoxic T lymphocytes (CTLs)
IL8↑,

Akk,

The Emerging Biotherapeutic Agent: Akkermansia

Review,

Var,

GutMicro↑, prebiotics, which promote the abundance of Akkermansia, is critical in preventing diseased conditions.

5351-

Akk,

Akkermansia muciniphila supplementation in patients with overweight/obese type 2 diabetes: Efficacy depends on its baseline levels in the gut

Human,

Diabetic,

GutMicro↑, AKK-WST01 supplementation successfully colonizes in low A. muciniphila participants
Weight↓, AKK-WST01 improves weight and metabolism in low A. muciniphila patients with T2D

5356-

AL,

Therapeutic role of allicin in gastrointestinal cancers: mechanisms and safety aspects

Review,

GC,

Apoptosis↑, induction of apoptosis, inhibition of proliferation, and disruption of cancer cell signaling pathways, including the MAPK, PI3K/AKT, and NF-κB pathways.
TumCP↓,
MAPK↓,
PI3K↓,
Akt↓,
NF-kB↓,
AntiCan↑, Allicin and its other derivatives, such as diallyl disulfide (DADS) and ajoene, have been found to have strong anticancer potential both in vitro and in vivo.
ChemoSen↑, effectiveness of allicin in augmenting conventional chemotherapy and retarding tumor growth proves that allicin is one of the most efficient complementary therapies.
TumCCA↑, In liver cancer, allicin has been shown to mediate cell cycle arrest and apoptosis
Apoptosis↑,
BioAv↑, Allicin (diallyl thiosulfinate) is a compound that is generated when a garlic clove is crushed
selectivity↑, Furthermore, it has no influence on the growth of healthy intestinal cells when it causes stomach cancer cells to undergo apoptosis
TGF-β↓, Allicin can reduce the production of TGF-β2 and its receptor after directly entering gastric cancer cells.
ROS↑, It induces oxidative stress by generating reactive oxygen species (ROS), leading to DNA damage and activation of key apoptotic mediators such as phospho-p53 and p21 [81].
DNAdam↑,
p‑P53↑,
P21↑,
cycD1/CCND1↓, Additionally, cyclin D1, cyclin E, and cyclin-dependent kinases (CDKs) can all be inhibited by allicin.
cycE/CCNE↓,
CDK4↓, suppressing the CDK-4/6/cyclin D complex
CDK6↓,
MMP↓, By lowering the outer mitochondrial membrane potential (MMP), allicin raises levels of nuclear factor kappa B (NF-κB), the proapoptotic protein Bax, while decreasing the antiapoptotic protein Bcl-2, which leads to apoptosis.
NF-kB↑,
BAX↑,
Bcl-2↓,
ER Stress↑, cellular effects of allicin, including its role in inducing ER stress
Casp↑, enhancing caspase activation and apoptosis-inducing factor (AIF)-mediated cell death.
AIF↑,
Fas↑, increasing Fas receptor expression and its binding to Fas ligand (FasL), leading to apoptosis through caspase-8 and cytochrome c activation.
Casp8↑,
Cyt‑c↑,
cl‑PARP↑, leading to poly (ADP-ribose) polymerase (PARP) cleavage and DNA fragmentation.
Ca+2↑, allicin elevates intracellular free Ca2⁺ levels, causing endoplasmic reticulum (ER) stress, which plays a critical role in apoptosis induction
*NRF2↑, by activating the Nrf2 pathway via KLF9, allicin protects against arsenic trioxide-induced liver damage,
*chemoP↑, Additionally, allicin has shown promise in reducing hepatotoxicity caused by tamoxifen (TAM), a commonly used treatment for hormone-dependent breast cancer
*GutMicro↑, Shi et al. [85] found that allicin can ameliorate high-fat diet-induced obesity in mice by altering their gut microbiome.
CycB/CCNB1↑, DATS impaired cell survival in the G2 phase by significantly upregulating cyclins A2 and B1.
H2S↑, DATS can also react with the cellular thiol glutathione to create H2S gas, which can control several other cellular functions [79].
HIF-1↓, allicin treatment (40 µg/ml) for NSCLC lowers the expression of HIF-1 and HIF-2 in hypoxic cells [73]
RadioS↑, Allicin has been shown to increase the sensitivity of X-ray radiation therapy in colorectal cancer, presumably by suppressing the levels of NF-κB, IKKβ mRNA, p-NF-κB, and p-IKKβ protein expression in vitro and in vivo

2660-

AL,

Allicin: A review of its important pharmacological activities

Review,

AD,

Review,

Var,

Review,

Park,

Review,

Stroke,

*Inflam↓, It showed neuroprotective effects, exhibited anti-inflammatory properties, demonstrated anticancer activity, acted as an antioxidant, provided cardioprotection, exerted antidiabetic effects, and offered hepatoprotection.
AntiCan↑,
*antiOx↑,
*cardioP↑, This vasodilatory effect helps protect against cardiovascular diseases by reducing the risk of hypertension and atherosclerosis.
*hepatoP↑,
*BBB↑, This allows allicin to easily traverse phospholipid bilayers and the blood-brain barrier
*Half-Life↝, biological half-life of allicin is estimated to be approximately one year at 4°C. However, it should be noted that its half-life may differ when it is dissolved in different solvents, such as vegetable oil
*H2S↑, allicin undergoes metabolism in the body, leading to the release of hydrogen sulfide (H2S)
*BP↓, H2S acts as a vasodilator, meaning it relaxes and widens blood vessels, promoting blood flow and reducing blood pressure.
*neuroP↑, It acts as a neuromodulator, regulating synaptic transmission and neuronal excitability.
*cognitive↑, Studies have suggested that H2S may enhance cognitive function and protect against neurodegenerative diseases like Alzheimer's and Parkinson's by promoting neuronal survival and reducing oxidative stress.
*neuroP↑, various research studies suggest that the neuroprotective mechanisms of allicin can be attributed to its antioxidant and anti-inflammatory properties
*ROS↓,
*GutMicro↑, may contribute to the overall health of the gut microbiota.
*LDH↓, Liu et al. found that allicin treatment led to a significant decrease in the release of lactate dehydrogenase (LDH),
*ROS↓, allicin's capacity to lower the production of reactive oxygen species (ROS), decrease lipid peroxidation, and maintain the activities of antioxidant enzymes
*lipid-P↓,
*antiOx↑,
*other↑, allicin was found to enhance the expression of sphingosine kinases 2 (Sphk2), which is considered a neuroprotective mechanism in ischemic stroke
*PI3K↓, allicin downregulated the PI3K/Akt/nuclear factor-kappa B (NF-κB) pathway, inhibiting the overproduction of NO, iNOS, prostaglandin E2, cyclooxygenase-2, interleukin-6, and tumor necrosis factor-alpha induced by interleukin-1 (IL-1)
*Akt↓,
*NF-kB↓,
*NO↓,
*iNOS↓,
*PGE2↓,
*COX2↓,
*IL6↓,
*TNF-α↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
*MPO↓, Furthermore, allicin significantly decreased tumor necrosis factor-alpha (TNF-α) levels and myeloperoxidase (MPO) activity, indicating its neuroprotective effect against brain ischemia via an anti-inflammatory pathway
*eff↑, Allicin, in combination with melatonin, demonstrated a marked reduction in the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2), Kelch-like ECH-associated protein 1 (Keap-1), and NF-κB genes in rats with brain damage induced by acryl
*NRF2↑, Allicin treatment decreased oxidative stress by upregulating Nrf2 protein and downregulating Keap-1 expression.
*Keap1↓,
*TBARS↓, It significantly reduced myeloperoxidase (MPO) and thiobarbituric acid reactive substances (TBARS) levels,
*creat↓, and decreased blood urea nitrogen (BUN), creatinine, LDH, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) levels.
*LDH↓,
*AST↓,
*ALAT↓,
*MDA↓,
*SOD↑, Allicin also increased the activity of superoxide dismutase (SOD) as well as the levels of glutathione S-transferase (GST) and glutathione (GSH) in the liver, kidneys, and brain
*GSH↑,
*GSTs↑,
*memory↑, Allicin has demonstrated its ability to improve learning and memory deficits caused by lead acetate injury by promoting hippocampal astrocyte differentiation.
chemoP↑, Allicin safeguards mitochondria from damage, prevents the release of cytochrome c, and decreases the expression of pro-apoptotic factors (Bax, cleaved caspase-9, cleaved caspase-3, and p53) typically activated by cisplatin
IL8↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
Cyt‑c↑, In addition, allicin was reported to induce cytochrome c, increase expression of caspase 3 [86], caspase 8, 9 [82,87], caspase 12 [80] along with enhanced p38 protein expression levels [81], Fas expression levels [82].
Casp3↑,
Casp8↑,
Casp9↑,
Casp12↑,
p38↑,
Fas↑,
P53↑, Also, significantly increased p53, p21, and CHK1 expression levels decreased cyclin B after allicin treatment.
P21↑,
CHK1↓,
CycB/CCNB1↓,
GSH↓, Depletion of GSH and alterations in intracellular redox status have been found to trigger activation of the mitochondrial apoptotic pathway was the antiproliferative function of allicin
ROS↑, Hepatocellular carcinoma (HCC) cells were sensitised by allicin to the mitochondrial ROS-mediated apoptosis induced by 5-fluorouracil
TumCCA↑, According to research findings, allicin has been shown to decrease the percentage of cells in the G0/G1 and S phases [87], while causing cell cycle arrest at the G2/M phase
Hif1a↓, Allicin treatment was found to effectively reduce HIF-1α protein levels, leading to decreased expression of Bcl-2 and VEGF, and suppressing the colony formation capacity and cell migration rate of cancer cells
Bcl-2↓,
VEGF↓,
TumCMig↓,
STAT3↓, antitumor properties of allicin have been attributed to various mechanisms, including promotion of apoptosis, inhibition of STAT3 signaling
VEGFR2↓, suppression of VEGFR2 and FAK phosphorylation
p‑FAK↓,

2667-

AL,

Allicin in Digestive System Cancer: From Biological Effects to Clinical Treatment

Review,

GC,

AntiCan↑, Allicin not only protects against tumors but also alleviates the adverse effects of anticancer treatment and enhances the chemotherapeutic response under certain conditions.
ChemoSen↑,
angioG↓, DATS works against tumors by blocking the cell cycle, inhibiting tumor cell proliferation, and inhibiting angiogenesis
chemoP↑,
*GutMicro↑, In addition to against bacteria, allicin has also been shown to modulate the composition of gut microbiota (GM) and increase the diversity of beneficial bacteria in animal models
*antiOx↑, allicin was confirmed to have strong antioxidant properties
other↝, Allicin is a reactive sulfur species (RSS) and a potent thiol-trapping reagent, rapidly reacting with glutathione (GSH) to yield S-allylmercaptoglutathione (GSSA)
GSH↓, Thus, allicin depletes the intracellular GSH pool and reacts with cysteine thiols available in proteins through S-thioallylation
Thiols↓, This reaction is the key to the biological activity of allicin, and the reversible oxidation and reduction of protein-thiols is the core of many processes in cells
*ROS↓, In a hypertrophic heart mouse model, the clearance of intracellular ROS by allicin was measured, and has been shown to reduce the production of ROS and block ROS-dependent ERK1/2, JNK1/2, AKT, NF-κB and Smad signaling, which leads to the inhibition o
*hepatoP↑, Moreover, allicin has been proven to play a hepatoprotective role against acetaminophen (APAP)-induced liver injury by reducing oxidative stress
*Inflam↓, OSCs in garlic has been shown to inhibit the tumor-mediated pro-inflammatory activity by modulating the cytokine pattern in a way that leads to an overall inhibition of NF-κB
*NF-kB↓,

3443-

ALA,

Molecular and Therapeutic Insights of Alpha-Lipoic Acid as a Potential Molecule for Disease Prevention

Review,

Var,

Review,

AD,

*antiOx↑, antioxidant potential and free radical scavenging activity.
*ROS↓,
*IronCh↑, Lipoic acid acts as a chelating agent for metal ions, a quenching agent for reactive oxygen species, and a reducing agent for the oxidized form of glutathione and vitamins C and E.
*cognitive↑, α-Lipoic acid enantiomers and its reduced form have antioxidant, cognitive, cardiovascular, detoxifying, anti-aging, dietary supplement, anti-cancer, neuroprotective, antimicrobial, and anti-inflammatory properties.
*cardioP↓,
AntiCan↑,
*neuroP↑,
*Inflam↓, α-Lipoic acid can reduce inflammatory markers in patients with heart disease
*BioAv↓, bioavailability in its pure form is low (approximately 30%).
*AntiAge↑, As a dietary supplements α-lipoic acid has become a common ingredient in regular products like anti-aging supplements and multivitamin formulations
*Half-Life↓, it has a half-life (t1/2) of 30 min to 1 h.
*BioAv↝, It should be stored in a cool, dark, and dry environment, at 0 °C for short-term storage (few days to weeks) and at − 20 °C for long-term storage (few months to years).
other↝, Remarkably, neither α-lipoic acid nor dihydrolipoic acid can scavenge hydrogen peroxide, possibly the most abundant second messenger ROS, in the absence of enzymatic catalysis.
EGFR↓, α-Lipoic acid inhibits cell proliferation via the epidermal growth factor receptor (EGFR) and the protein kinase B (PKB), also known as the Akt signaling, and induces apoptosis in human breast cancer cells
Akt↓,
ROS↓, α-Lipoic acid tramps the ROS followed by arrest in the G1 phase of the cell cycle and activates p27 (kip1)-dependent cell cycle arrest via changing of the ratio of the apoptotic-related protein Bax/Bcl-2
TumCCA↑,
p27↑,
PDH↑, α-Lipoic acid drives pyruvate dehydrogenase by downregulating aerobic glycolysis and activation of apoptosis in breast cancer cells, lactate production
Glycolysis↓,
ROS↑, HT-29 human colon cancer cells; It was concluded that α-lipoic acid induces apoptosis by a pro-oxidant mechanism triggered by an escalated uptake of mitochondrial substrates in oxidizable form
*eff↑, Several studies have found that combining α-lipoic acid and omega-3 fatty acids has a synergistic effect in slowing functional and cognitive decline in Alzheimer’s disease
*memory↑, α-lipoic acid inhibits brain weight loss, downregulates oxidative tissue damage resulting in neuronal cell loss, repairs memory and motor function,
*motorD↑,
*GutMicro↑, modulates the gut microbiota without reducing the microbial diversity (

5409-

ASA,

Role of aspirin in cancer prevention

Review,

Var,

Imm↑, It was proved that aspirin showed advantages in immunomodulation, cell metabolism, gene repair, reduction of inflammatory reaction, anti-platelet activation and improvement of intestinal flora.
*Inflam↓,
*AntiAg↑, Clinicians have found that aspirin not only has anti-platelet aggregation, antipyretic, and analgesic effects, but also has a potential additional effect on the prevention and treatment of cancer.
*GutMicro↑,
eff↑, combination of aspirin and existing anti-tumor drugs also showed some synergistic effects.
TumMeta↓, The results showed that the aspirin group decreased the rate of distant metastasis, especially for colorectal cancer [3].
angioG↓, Studies have shown that aspirin can bind directly to the GLU150(Q9y251: Glu 225) region to inhibit heparanase activity and regulate related signalling pathways, thereby inhibiting angiogenesis and tumour metastasis [4].
Risk↓, A study published in the JAMA Network Open suggested that frequent aspirin use (defined as daily or almost daily use for 6 months or longer) was associated with a 13 % lower risk of ovarian cancer, and this protective association was not affected by
Risk↓, 1982 to 2009, and it was found that compared with non-aspirin users, men who take aspirin regularly (more than three tablets per week) have a lower risk of fatal prostate cancer.

5421-

ASTX,

Astaxanthin Inhibits PC-3 Xenograft Prostate Tumor Growth in Nude Mice

in-vivo,

Pca,

Nude Mice

TumCG↑, 100 mg/kg astaxanthin significantly inhibited tumor growth compared to the TC group, with an inhibitory rate of 41.7%.
Ki-67↑, A decrease of Ki67 and proliferating cell nuclear antigen (PCNA) as well as an increase of cleaved caspase-3 were observed in HA-treated tumors
PCNA↓,
GutMicro↑, The HA significantly elevated the levels of tumor suppressors miR-375 and miR-487b in tumor tissues and the amount of Lactobacillus sp. and Lachnospiraceae in mice stools, while there was no significant difference between LA and TC groups.
*Inflam↓, Dietary supplementation with astaxanthin was reported to exert beneficial effects against inflammation, cardiovascular disease, and oxidative damage, suggesting that astaxanthin is a functional food ingredient
*cardioP↑,
*ROS↓,

5424-

ASTX,

Astaxanthin exerts an adjunctive anti-cancer effect through the modulation of gut microbiota and mucosal immunity

in-vivo,

Nor,

mice

*GutMicro↑, Astaxanthin synergistically enhances the anticancer effects of sorafenib by modulating intestinal flora.
AntiCan↑,
eff↑, Astaxanthin significantly promotes the proliferation of Akkermansia, a microorganism with enhanced anti-tumor immune effects.
AntiTum↑, Therefore, it strengthens the body's anti-tumor immune response and synergistically boosts the therapeutic efficacy of drugs.
ChemoSen↑,

4982-

ATV,

Inhibiting the mevalonate pathway with atorvastatin alters gut microbiota and has potential as an anti-cancer treatment for ovarian cancer

in-vivo,

Ovarian,

Female C57BL/6 mice

HMG-CoA↓, Statins, a mevalonate (MVA) pathway antagonist, are widely used to treat and prevent hypercholesterolemia by blocking cellular production of cholesterol.
GutMicro↑, Furthermore, statins have been shown to induce significant changes in intestinal enterotypes in both humans and mice. statins favorably alter the intestinal microbiome

5365-

AV,

Aloe Vera Polysaccharides as Therapeutic Agents: Benefits Versus Side Effects in Biomedical Applications

Review,

Nor,

Review,

IBD,

Review,

Diabetic,

*Wound Healing↑, Traditionally recognized for its anti-inflammatory and antimicrobial effects, which are very important in wound healing, the Aloe Vera relies on its polysaccharides
*Imm↑, which confer immunomodulatory, antioxidant, and tissue-regenerative properties.
*antiOx↑,
*AntiDiabetic↑, graphical abstract
*AntiCan↑,
*Inflam↓, The anti-inflammatory properties of Aloe Vera polysaccharides are primarily mediated through the inhibition of key inflammatory pathways.
*NF-kB↓, Acemannan and other polysaccharides suppress the activation of nuclear factor-kappa B (NF-κB), a transcription factor that regulates the expression of pro-inflammatory genes.
*COX2↓, By inhibiting NF-κB [48,49], Aloe Vera polysaccharides reduce the production of cyclooxygenase-2 (COX-2) and lipoxygenase (LOX),
*5LO↓,
*IL1β↓, Aloe Vera polysaccharides downregulate the expression of pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α, while upregulating anti-inflammatory cytokines such as IL-10
*IL6↓,
*TNF-α↓,
*IL10↑,
*other↓, This dual action helps to mitigate inflammation in conditions such as arthritis, dermatitis, and inflammatory bowel disease (IBD)
*ROS↓, Aloe Vera polysaccharides exhibit potent antioxidant activity by scavenging reactive oxygen species (ROS) and free radicals,
*SOD↑, The polysaccharides enhance the activity of endogenous antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), which neutralize oxidative stress and protect cells from damage [17,63].
*Catalase↑,
*GPx↑,
*lipid-P↓, This property is particularly beneficial in preventing lipid peroxidation, DNA damage, and protein oxidation, processes associated with chronic diseases and aging
*DNAdam↓,
*GutMicro↑, Aloe Vera polysaccharides support gastrointestinal health, acting as prebiotics and promoting the growth of beneficial gut microbiota such as Lactobacillus and Bifidobacterium species [64].
*ZO-1↑, enhance the integrity of the intestinal epithelial barrier by upregulating the expression of tight junction proteins such as occludin and zonula occludens-1 (ZO-1) [51,54].
AntiTum↑, Certain polysaccharides in Aloe Vera, including acemannan, have demonstrated antitumoral effects by inducing apoptosis (programmed cell death) in cancer cells.
Casp3↑, This is achieved through the activation of caspase-3 and caspase-9, key enzymes in the apoptotic pathway [45,48].
Casp9↑,
angioG↓, Aloe Vera polysaccharides also inhibit angiogenesis and metastasis by downregulating matrix metalloproteinases (MMPs) and VEGF [75].
MMPs↓,
VEGF↓,
NK cell↑, Moreover, these polysaccharides enhance the immune system’s ability to recognize and destroy cancer cells through stimulating natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) [43,55].

5571-

B-Gluc,

immuno,

Potential benefit of β-glucans as adjuvant therapy in immuno-oncology: a review

Review,

Var,

Imm↑, In this way, β-glucans can be exploited as adjuvant cancer therapy, in particular by a synergic action with chemotherapy or immunotherapy
ChemoSen↑, t has been demonstrated that the association of β-glucans with chemotherapy is able to enhance cytotoxicity and can improve patient clinical outcome.
LDL↑, mechanism that rules the cholesterol-lowering effects of β-glucans takes place through the gut microbiota and the production of short-chain fatty acids (SCFAs, for example propionate).
GutMicro↑,
TumCP↓, In the oncological field, β-glucans can stimulate the innate and adaptive immune response, inhibit the proliferation of cancer cells, promote apoptosis and block the angiogenesis [24–26].
Apoptosis↑,
angioG↓,
QoL↑, In this way, β-glucan demonstrate synergic effect with antitumor mAbs agents and they can have an important role to improve the therapeutic effects and the quality of life in cancer patients.

5574-

B-Gluc,

Beta Glucan: Health Benefits in Obesity and Metabolic Syndrome

Review,

Obesity,

*BioAv↑, β-glucan is a relatively inexpensive milling byproduct, and it is added to foods on the assumption that this will contribute to health benefits.
*toxicity↓, Moreover, no human adverse effects have been reported following the consumption of a diet rich in β-glucan from oat or barley flour or their extracts [70].
*Imm↑, Among polysaccharides that act as immunostimulants, β-glucans were found to be the most effective against infectious diseases and cancer [88].
*eff↑, The immunological potency of β-glucans varies with the molecular mass, solution conformation, backbone structure, degree of branching as well as the cell type that is targeted [89].
*Risk↓, pretreatment of high-risk surgical patients with intravenous yeast β-(1,3; 1,6)-D-glucan decreased the infection incidence, shortened intensive care unit length stay, and improved survival in comparison to a saline placebo injection
*Weight↓, In this particular study, chitin-glucan decreased high fat diet-induced body weight gain, fat mass development, fasting hyperglycemia, glucose intolerance,
*eff↝, A drink containing 5 g of oat β-glucan with a molecular weight 70 000 Da significantly lowered postprandial glucose and insulin levels relative to a rice drink control, while a similar drink containing barley β-glucan 40 000 Da had no effect
*BP↓, 8 g/day of supplemented soluble fiber from oat bran over 12 weeks significantly reduced both systolic and diastolic blood pressure in comparison to the control [197].
*GutMicro↑, Beta glucans selectively support the growth of Lactobacilli and Bifidobacteria, both of them being antagonists to pathogenic bacteria in the digestive system [
*eff↓, freeze-thaw cycle reduced the solubility of β-glucan in oat bran muffins by 9% to 55% of the fresh values.

5577-

B-Gluc,

Lentinan progress in inflammatory diseases and tumor diseases

Review,

Var,

Review,

IBD,

AntiTum↑, LNT are macromolecules with a β-1,3-D-glucan and its unique molecular structure is closely related to its pharmacological activity, and the glucan of the β-glycosidic bond is the key structure for its antitumor function [6, 7].
GutMicro↑, LNT could also improve the imbalance of gut microbial colonies [25].
*Inflam↓, LNT exerts its anti-inflammatory effect by downregulating cell surface TNFR1 to inhibit TNF-α-induced NF-κB activation
*TNF-α↓,
*NF-kB↓,
ChemoSen↑, LNT combined with cisplatin can not only reduce the dose of cisplatin, but also promote the activation of the intrinsic apoptosis pathway through the regulation of signals, leading to apoptosis of liver cancer cells
OS↑, LNT combined with pentafluorouracil improved survival time for advanced gastric cancer, which is consistent with the results of a meta-study of five randomized controlled trials [78, 79].
Imm↑, Although LNT has been approved in Japan as an immune agent for chemotherapy in gastric cancer
IL6↓, significantly enhance the immune function of CD4 cells, increase NK cells and reduce IL-6 levels
ERK↓, Studies have shown that LNT can inhibit the ERK/MAPK signaling pathway by regulating miR-340, thereby promoting apoptosis in osteosarcoma cells
MAPK↓,
*antiOx↑, LNT is an shiitake extract with anti-inflammatory, antioxidant, anti-tumor and other biological activities and functions.
eff↑, Furthermore,studies also found that LNT selenium nanoparticles can promote apoptosis by acting on specific signaling pathways [96, 97].

2769-

Ba,

Rad,

Baicalein ameliorates ionizing radiation-induced injuries by rebalancing gut microbiota and inhibiting apoptosis

in-vivo,

Nor,

MICE

*radioP↑, Baicalein rebalances gut microbial composition pattern destroyed by irradiation. upport the potential of baicalein as a radioprotective medicine
GutMicro↑,
*P53↓, baicalein inhibited the activation of p53 and p53 mediated mitochondrial apoptosis and death receptor apoptosis in the intestine.
*Apoptosis↑,
*DR4↓,

2605-

Ba,

BA,

Potential therapeutic effects of baicalin and baicalein

Review,

Var,

Review,

Stroke,

Review,

IBD,

Review,

Arthritis,

Review,

AD,

Review,

Park,

cardioP↑, cardioprotective activities.
Inflam↓, Decreasing the accumulation of inflammatory mediators and improving cognitive function
cognitive↑,
*hepatoP↑, Decreasing inflammation, reducing oxidative stress, regulating the metabolism of lipids, and decreasing fibrosis, apoptosis, and steatosis are their main hepatoprotective mechanisms
*ROS?, Reducing oxidative stress and protecting the mitochondria to inhibit apoptosis are proposed as hepatoprotective mechanisms of baicalin in NAFLD
*SOD↑, Baicalin could reduce the levels of ROS and fatty acid-induced MDA, and increase superoxide dismutase (SOD) and glutathione amounts compared to the control.
*GSH↑,
*MMP↑, Moreover, baicalin could partially restore mitochondrial morphology and increase ATP5A expression and mitochondrial membrane potential (Gao et al., 2022).
*GutMicro↑, After baicalein treatment, a remodelling in the overall structure of the gut microbiota was observed
ChemoSen↑, Besides, a combination of baicalin and doxorubicin could elevate the chemosensitivity of MCF-7 and MDA-MB-231 breast cancer cells
*TNF-α↓, Baicalin can protect cardiomyocytes from hypoxia/reoxygenation injury by elevating the SOD activity and anti-inflammatory responses through reducing TNF-α, enhancing IL-10 levels, decreasing IL-6, and inhibiting the translocation of NF-κB to the nucl
*IL10↑,
*IL6↓,
*eff↑, Studies show that baicalin and baicalein may be effective against IBD by suppressing oxidative stress and inflammation, and regulating the immune system.
*ROS↓,
*COX2↓, baicalein can improve the symptoms of ulcerative colitis by lowering the expression of pregnane X receptor (PXR), (iNOS), (COX-2), and caudal-type homeobox 2 (Cdx2), as well as the NF-κβ and STAT3
*NF-kB↓,
*STAT3↓,
*PGE2↓, Administration of baicalin (30-90 mg/kg) could decrease the levels of prostaglandin E2 (PEG2), myeloperoxidase (MPO), IL-1β, TNF-α, and the apoptosis-related genes including Bcl-2 and caspase-9
*MPO↓,
*IL1β↓,
*MMP2↓, Rheumatoid arthritis RA mouse model by supressing relevant proinflammatory cytokines such as IL-1b, IL-6, MMP-2, MMP-9, TNF-α, iNOS, and COX-2)
*MMP9↓,
*β-Amyloid↓, Alzheimer’s disease (AD) : reduce β-amyloid and trigger non-amyloidogenic amyloid precursor proteins.
*neuroP↑, For instance, administration of baicalin orally for 14 days (100 mg/kg body weight) exhibited neuroprotective effects on pathological changes and behavioral deficits of Aβ 1–42 protein-induced AD in vivo.
*Dose↝, administration of baicalin (500 mg/day, orally for 12 weeks) could improve the levels of total cholesterol, TGs, LDLC and apolipoproteins (APOs), and high-sensitivity C-reactive protein (hs-CRP) in patients with rheumatoid arthritis and coronary arte
*BioAv↝, the total absorption of baicalin depends on the activity of intestinal bacteria to convert baicalin to baicalein as the first step.
*BioAv↝, Kidneys, liver, and lungs are the main organs in which baicalin accumulates the most.
*BBB↑, Baicalin and baicalein can pass through the blood brain barrier (BBB)
*BDNF↑, mechanism of action for baicalein is illustrated in Figure 3. Activation of the BDNF/TrkB/CREB pathway, inhibition of NLRP3/Caspase-1/GSDMD pathway,

2712-

BBR,

Suppression of colon cancer growth by berberine mediated by the intestinal microbiota and the suppression of DNA methyltransferases (DNMTs)

in-vitro,

Colon,

HT29

in-vivo,

NA,

TumCG↓, BBR reduced the growth of colon cancer cells to a certain extent in vitro and in vivo,
GutMicro↑, BBR significantly mediated the abundance, composition and metabolic functions of the intestinal microbial flora in mice with colon cancer
other↝, The effect of BBR on inflammatory cytokines, including IL-6, FGF, and PDGF, was not obvious
IL10↓, BBR significantly downregulated IL-10 levels (P < 0.05) and reduced c-Myc, DNMT1, and DNMT3B
cMyc↓,
DNMT1↓,
DNMTs↓,

2713-

BBR,

Berberine improved the microbiota in lung tissue of colon cancer and reversed the bronchial epithelial cell changes caused by cancer cells

in-vitro,

Nor,

BEAS-2B

Thirty-six BALB/c nude mice

*GutMicro↑, Berberine or probiotics significantly increased the alpha diversity of the lung microbiota
*IL6↑, Berberine increased IL-6 and IL-10 and decreased IL-17 and IFN-γ expression in lung tissue
*IL10↑,
*IL17↑,
*IFN-γ↑,
PDGF↓, In addition, HT29 and RKO CM had no significant effect on the expression of PDGF-β in BEAS-2B cells, while berberine significantly reduced its expression.
*RAD51↓, berberine protects lung cells against this stress by enhancing RAD51 expression.

2678-

BBR,

Berberine as a Potential Agent for the Treatment of Colorectal Cancer

Review,

CRC,

*Inflam↓, BBR exerts remarkable anti-inflammatory (94–96), antiviral (97), antioxidant (98), antidiabetic (99), immunosuppressive (100), cardiovascular (101, 102), and neuroprotective (103) activities.
*antiOx↑,
*cardioP↑,
*neuroP↑,
TumCCA↑, BBR could induce G1 cycle arrest in A549 lung cancer cells by decreasing the levels of cyclin D1 and cyclin E1
cycD1/CCND1↓,
cycE/CCNE↓,
CDC2↓, BBR also induced G1 cycle arrest by inhibiting cyclin B1 expression and CDC2 kinase in some cancer cells
AMPK↝, BBR has been suggested to induce autophagy in glioblastoma by targeting the AMP-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR)/ULK1 pathway
mTOR↝,
Casp8↑, BBR has been revealed to stimulate apoptosis in leukemia by upregulation of caspase-8 and caspase-9
Casp9↑,
Cyt‑c↑, in skin squamous cell carcinoma A431 cells by increasing cytochrome C levels
TumCMig↓, BBR has been confirmed to inhibit cell migration and invasion by inhibiting the expression of epithelial–mesenchymal transition (EMT)
TumCI↓,
EMT↓,
MMPs↓, metastasis-related proteins, such as matrix metalloproteinases (MMPs) and E-cadherin,
E-cadherin↓,
Telomerase↓, BBR has shown antitumor effects by interacting with microRNAs (125) and inhibiting telomerase activity
*toxicity↓, Numerous studies have revealed that BBR is a safe and effective treatment for CRC
GRP78/BiP↓, Downregulates GRP78
EGFR↓, Downregulates EGFR
CDK4↓, downregulates CDK4, TERT, and TERC
COX2↓, Reduces levels of COX-2/PGE2, phosphorylation of JAK2 and STAT3, and expression of MMP-2/-9.
PGE2↓,
p‑JAK2↓,
p‑STAT3↓,
MMP2↓,
MMP9↓,
GutMicro↑, BBR can inhibit tumor growth through meditation of the intestinal flora and mucosal barrier, and generally and ultimately improve weight loss. BBR has been reported to modulate the composition of intestinal flora and significantly reduce flora divers
eff↝, BBR can regulate the activity of P-glycoprotein (P-gp), and potential drug-drug interactions (DDIs) are observed when BBR is coadministered with P-gp substrates
*BioAv↓, the efficiency of BBR is limited by its low bioavailability due to its poor absorption rate in the gut, low solubility in water, and fast metabolism. Studies have shown that the oral bioavailability of BBR is 0.68% in rats
BioAv↑, combining it with p-gp inhibitors (such as tariquidar and tetrandrine) (196, 198), and modification to berberine organic acid salts (BOAs)

5621-

Bif,

immuno,

Commensal Bifidobacterium promotes antitumor immunity and facilitates anti–PD-L1 efficacy

TumCG↓, Oral administration of Bifidobacterium alone improved tumor control to the same degree as programmed cell death protein 1 ligand 1 (PD-L1)–specific antibody therapy (checkpoint blockade), and combination treatment nearly abolished tumor outgrowth.
GutMicro↑, Our data suggest that manipulating the microbiota may modulate cancer immunotherapy.

5623-

Bif,

Bifidobacterium breve predicts the efficacy of anti-PD-1 immunotherapy combined with chemotherapy in Chinese NSCLC patients

Study,

NSCLC,

Fecal samples from 21 non‐small cell lung cancer (NSCLC) patients and 22 healthy volunteers

GutMicro↑, Bifidobacterium, Escherichia, and Sarterella were significantly enriched in patients with clinical benefit response (p < 0.05), and these three bacteria had certain predictive value for clinical benefit.
OS↑, Patients with Bifidobacterium breve had significantly longer median progression‐free survival (mPFS) compared with patients with no detectable Bifidobacterium breve feces at baseline (106 days vs. NR, p < 0.001).
eff↑, The clinical efficacy of anti‐PD‐1 therapy combined with chemo in Chinese advanced NSCLC patients is closely related to the gut microbiota, and Bifidobacterium breve may be a potential biomarker to predict the efficacy of immune‐combined chemo

5628-

Bif,

immuno,

Bifidobacterium modulation of tumor immunotherapy and its mechanism

Review,

Var,

Imm↑, his review will focus on the immunomodulatory effects of Bifidobacteria in malignancies and the possible mechanisms of action of Bifidobacteria on immunotherapy
Risk↓, Bifidobacteria have a role in the prevention of intestinal cancer in healthy intestinal microbiota by influencing intestinal probiotics metabolism and enhancing the host immune response;
GutMicro↑,
AntiTum↑, Bifidobacteria has been shown to positively induce an anti-tumor immune response [32].
OS↑, Bifidobacterium longum 420 significantly increased the survival of mice carrying renal cell carcinoma tumors treated with anti-PD-1 and anti-CTLA-4 antibodies
selectivity↑, Bifidobacteria have been shown to selectively accumulate in tumors upon entry into the blood stream, possibly due to the hypoxic microenvironment’s
eff↑, (e.g., probiotic strains such as Bifidobacterium bifidum) to enhance the efficacy of cancer immunotherapy is still in its infancy,

5629-

Bif,

ProBio,

Gut microbiota shapes cancer immunotherapy responses

Review,

Var,

eff↑, oral administration of Bifidobacterium enhanced the anti-tumor efficacy of PD-L1 inhibitors by promoting dendritic cell (DC) maturation and increasing tumor-specific CD8 + T cell activity.
DCells↑,
CD8+↑,
eff↑, One study analyzing plasma samples from colorectal cancer (CRC) patients treated with ACT and chemotherapy found that responders had significantly higher blood levels of Bifidobacterium, Lactobacillus, and Enterococcus, indicating that the blood micr
AntiTum↑, Inosine, a purine metabolite produced by Akkermansia muciniphila and Bifidobacterium longum, enhances antitumor immunity by inhibiting UBA6 expression in tumor cells,
other↑, Likewise, vitamin B6, synthesized by Lactobacillus acidophilus and Bifidobacterium bifidum, boosts T lymphocyte proliferation and promotes antitumor immunity by stimulating T cell activity
selectivity↑, Additionally, Bifidobacterium preferentially accumulates in tumors . Bifidobacterium, for example, migrates to colonize and enrich CRC tumors198
GutMicro↑, Microbiome analysis revealed enrichment of beneficial bacteria (Bifidobacterium longum, Lachnospiraceae, Ruminococcaceae) and a decline in potentially detrimental species such as Bacteroides.

752-

Bor,

The Potential Role of Boron in the Modulation of Gut Microbiota Composition: An In Vivo Pilot Study

GutMicro↑, Notable increases in genera like Treponema and Catellicoccus were observed, suggesting the potential of boron compounds to enrich microbial communities with unique metabolic functions

2776-

Bos,

Anti-inflammatory and anti-cancer activities of frankincense: Targets, treatments and toxicities

Review,

Var,

*5LO↓, Arthritis Human primary chondrocytes: 5-LOX↓, TNF-α↓, MMP3↓
*TNF-α↓,
*MMP3↓,
*COX1↓, COX-1↓, Leukotriene synthesis by 5-LOX↓
*COX2↓, Arthritis Human blood in vitro: COX-2↓, PGE2↓, TH1 cytokines↓, TH2 cytokines↑
*PGE2↓,
*Th2↑,
*Catalase↑, Ethanol-induced gastric ulcer: CAT↑, SOD↑, NO↑, PGE-2↑
*SOD↑,
*NO↑,
*PGE2↑,
*IL1β↓, inflammation Human PBMC, murine RAW264.7 macrophages: TNFα↓ IL-1β↓, IL-6↓, Th1 cytokines (IFNγ, IL-12)↓, Th2 cytokines (IL-4, IL-10)↑; iNOS↓, NO↓, phosphorylation of JNK and p38↓
*IL6↓,
*Th1 response↓,
*Th2↑,
*iNOS↓,
*NO↓,
*p‑JNK↓,
*p38↓,
GutMicro↑, colon carcinogenesis: gut microbiota; pAKT↓, GSK3β↓, cyclin D1↓
p‑Akt↓,
GSK‐3β↓,
cycD1/CCND1↓,
Akt↓, Prostate Ca: AKT and STAT3↓, stemness markers↓, androgen receptor↓, Sp1 promoter binding↓, p21(WAF1/CIP1)↑, cyclin D1↓, cyclin D2↓, DR5↑,CHOP↑, caspases-3/-8↑, PARP cleavage, NFκB↓, IKK↓, Bcl-2↓, Bcl-xL↓, caspase 3↑, DNA
STAT3↓,
CSCs↓,
AR↓,
P21↑,
DR5↑,
CHOP↑,
Casp3↑,
Casp8↑,
cl‑PARP↑,
DNAdam↑,
p‑RB1↓, Glioblastoma: pRB↓, FOXM1↓, PLK1↓, Aurora B/TOP2A pathway↓,CDC25C↓, pCDK1↓, cyclinB1↓, Aurora B↓, TOP2A↓, pERK-1/-2↓
FOXM1↓,
TOP2↓,
CDC25↓,
p‑CDK1↓,
p‑ERK↓,
MMP9↓, Pancreas Ca: Ki-67↓, CD31↓, COX-2↓, MMP-9↓, CXCR4↓, VEGF↓
VEGF↓,
angioG↓, Apoptosis↑, G2/M arrest, angiogenesis↓
ROS↑, ROS↑,
Cyt‑c↑, Leukemia : cytochrome c↑, AIF↑, SMAC/DIABLO↑, survivin↓, ICAD↓
AIF↑,
Diablo↑,
survivin↓,
ICAD↓,
ChemoSen↑, Breast Ca: enhancement in combination with doxorubicin
SOX9↓, SOX9↓
ER Stress↑, Cervix Ca : ER-stress protein GRP78↑, CHOP↑, calpain↑
GRP78/BiP↑,
cal2↓,
AMPK↓, Breast Ca: AMPK/mTOR signaling↓
mTOR↓,
ROS↓, Boswellia extracts and its phytochemicals reduced oxidative stress (in terms of inhibition of ROS and RNS generation)

5711-

Brut,

Citrus bergamia powder: Antioxidant, antimicrobial and anti-inflammatory properties

in-vitro,

Nor,

HMEC

*antiOx↑, Bergamot whole-fruit showed a high in vitro and ex vivo antioxidant activity.
*Bacteria↓, Bergamot extract exerted antibacterial activity against pathogenic bacteria.
*GutMicro↑, Bergamot extract slightly stimulated gut-beneficial bacteria.

5744-

Buty,

PacT,

Oral sodium butyrate supplementation ameliorates paclitaxel-induced behavioral and intestinal dysfunction

in-vivo,

Var,

 BuNa dissolved in drinking water (0.23 mg/ml)

mice

chemoP↑, Sodium butyrate attenuates paclitaxel-induced intestinal dysfunction and inflammation.
neuroP↑, The treatment with BuNa also ameliorated depressive- and anxiety-like behaviors induced by PTX in mice, and these effects were associated with neuroprotective and anti-inflammatory outcomes.
Inflam↓,
GutMicro↑, BuNa restored PTX-induced altered gut barrier integrity, microbiota composition and food intake suggesting a gut-to-brain communication.
*ROS↓, Butyrate maintains gut homeostasis by improving inflammation [52], [53], oxidative status [54] and epithelial barrier defense [55].
Dose↝, Assuming that mice drink an average of 4 ml/day, BuNa-treated water resulting in an estimated dose of 30 mg/kg/day.

5743-

Buty,

Regulation of Intestinal Butyrate Transporters by Oxidative and Inflammatory Status

Review,

Var,

*GutMicro↑, Beneficial effects of the microbiota-derived metabolite butyrate at the colonic level are well established, particularly through its relevance in colorectal cancer (CRC) and inflammatory bowel disease (IBD)
*other↑, (2) stimulates growth and proliferation of normal intestinal epithelial cells;
*Inflam↓, (3) inhibits inflammation;
*ROS↓, (4) inhibits oxidative stress;
AntiCan↑, (8) inhibits colon carcinogenesis
HCAR2↑, three cell-surface G-protein-coupled receptors, GPR41, GPR43, and GPR109A, are targets for butyrate [1,2].
HDAC↓, butyrate also has intracellular actions (HDAC inhibition),

5739-

Buty,

Butyrate as a promising therapeutic target in cancer: From pathogenesis to clinic (Review)

Review,

Var,

GutMicro↑, Butyrate, a short-chain fatty acid, is generated through gut microbial fermentation of dietary fiber.
*Inflam↓, Butyrate, a primary anti-inflammatory SCFA, exhibits a multifaceted role in mitigating inflammation
*IL6↓, It inhibits the production of pro-inflammatory cytokines and chemokines, such as IL-6, TNF-α and IL-17, which helps to prevent colon cancer
*TNF-α↓,
*IL17↓,
*IL10↑, while promoting IL-10 production
*ROS↝, regulates the production of reactive oxygen species (ROS)
COX2↓, butyrate has been observed to suppress inflammation by inhibiting the expression of cyclooxygenase-2 mRNA in colonic tissues (60).
NLRP3↓, butyrate exhibits the highest efficiency in the negative regulation of NLRP3
Imm↑, Enhancement of the immunotherapeutic effect
HDAC↓, Inhibition of HDAC activity in cells
TumCCA↑, Butyrate has been found to induce cell cycle arrest in the G0/G1 phase in a dose-dependent manner in vitro in numerous tumors, including colon, liver, lung and bladder cancer,
Apoptosis↑, butyrate-induced apoptosis is accompanied by elevated ROS levels and caspase activity (126)
ROS↑,
Casp↑,
mtDam↑, suggests that ROS can induce mitochondrial membrane damage, release Cyt c from damaged mitochondria, and enhance apoptosis via the Cyt c/caspase-3 pathway
Cyt‑c↑,
eff↑, Clostridium butyricum is an anaerobic bacterium classified as a probiotic due to its production of butyric acid (139)
chemoP↑, butyrate not only alleviates the side effects associated with conventional chemotherapeutic agents such as oxaliplatin, irinotecan and 5-fluorouracil (149-151), but it also enhances the efficacy of both chemotherapy and immunotherapy
ChemoSen↑,
eff↑, metformin has been demonstrated to enhance the biosynthesis of butyrate while concurrently inhibiting the progression of CRC
RadioS↑, Butyrate significantly enhanced radiation-induced cell death and enhanced treatment effects compared with administration of radiation alone.
HCAR2↑, Activation of cell-surface receptors (GPR41, GPR43 and GPR109A);

5738-

Buty,

Butyrate’s role in human health and the current progress towards its clinical application to treat gastrointestinal disease

Review,

Nor,

*GutMicro↑, Maintaining optimal butyrate levels improves gastrointestinal health in animal models by supporting colonocyte function, decreasing inflammation, maintaining the gut barrier, and promoting a healthy microbiome.
*Risk↓, Butyrate has also shown protective actions in the context of intestinal diseases such as inflammatory bowel disease, graft-versus-host disease of the gastrointestinal tract, and colon cancer,

5735-

Buty,

Butyrate and the Intestinal Epithelium: Modulation of Proliferation and Inflammation in Homeostasis and Disease

Study,

Nor,

*Inflam↓, Butyrate also regulates epithelial inflammation and tolerance to antigens, through production of anti-inflammatory cytokines and induction of tolerogenic dendritic cells
GutMicro↑, Several species of commensal Gram-positive bacteria in the colon possess the ability to synthesize butyrate, primarily from dietary starch and fiber,with the two most abundant groups appearing to be Faecalibacterium prausnitzii and Roseburia species
Imm↑, Butyrate as an Immunomodulator in the Intestine and Beyond

5733-

Buty,

VitB3,

Activation of Gpr109a, Receptor for Niacin and the Commensal Metabolite Butyrate, Suppresses Colonic Inflammation and Carcinogenesis

in-vivo,

CRC,

mice

GutMicro↑, Commensal gut microflora and dietary fiber protect against colonic inflammation and colon cancer through unknown targets. Butyrate, a bacterial product from fermentation of dietary fiber in the colon, has been implicated in this process
HCAR2↑, GPR109A is also a receptor for niacin, which is also produced by gut microbiota and suppresses intestinal inflammation.
AntiCan↑, Niacin, a pharmacological Gpr109a agonist, suppressed colitis and colon cancer in a Gpr109a-dependent manner.
Inflam↓, We hypothesized that GPR109A has an anti-inflammatory role in the colon.
IL18↑, Butyrate or Niacin Induces IL-18 Expression in Colonic Epithelium in a Gpr109a-Dependent Manner

5732-

Buty,

GPR109A is a G-protein-coupled receptor for the bacterial fermentation product butyrate and functions as a tumor suppressor in colon

Study,

CRC,

Human colonic biopsies were obtained during colonoscopy

HCAR2↑, Millimolar concentrations of butyrate are needed to activate the receptor.
other↓, The expression of GPR109A is silenced in colon cancer in humans, in a mouse model of intestinal/colon cancer, and in colon cancer cell lines.
Apoptosis↑, Re-expression of GPR109A in colon cancer cells induces apoptosis, but only in the presence of its ligands butyrate and nicotinate.
HDAC↓, Butyrate is an inhibitor of histone deacetylases, but apoptosis induced by activation of GPR109A with its ligands in colon cancer cells does not involve inhibition of histone deacetylation.
Bcl-2↓, primary changes in this apoptotic process include downregulation of Bcl-2, Bcl-xL, and cyclin D1, and upregulation of death receptor pathway.
Bcl-xL↓,
cycD1/CCND1↓,
DR5↑,
NF-kB↓, In addition, GPR109A/butyrate suppresses NF-κB activation in normal and cancer colon cell lines as well as in normal mouse colon.
GutMicro↑, Gut bacteria play a critical role in the prevention of colon cancer and inflammatory bowel disease
SLC12A5↝, We have shown previously that butyrate induces apoptosis in colon cancer cell lines if SLC5A8, a butyrate transporter, is expressed in these cells and that the process is associated with inhibition of HDACs

1032-

Buty,

Gut microbiome-derived butyrate inhibits the immunosuppressive factors PD-L1 and IL-10 in tumor-associated macrophages in gastric cancer

in-vivo,

GC,

AGS

human and mice

GutMicro↑, Restoration of the intestinal microbiome and its metabolic functions inhibit tumor growth The abundances of Faecalibacterium and Bifidobacterium in the intestinal flora were lower in GC patients than in healthy individuals.
PD-L1↓, Butyrate, a representative microbiome metabolite, suppressed the expression levels of PD-L1 and IL-10 in immune cells.
IL10↓,
TumCG↓, Butyrate inhibited tumor growth in mice

5859-

CAP,

Are We Ready to Recommend Capsaicin for Disorders Other Than Neuropathic Pain?

Review,

Var,

*TRPV1↑, the absorbed capsaicin activates its receptor TRPV1, which causes the rapid influx of sodium ions (Na+) and calcium (Ca2+) from the extracellular environment to the cell interior.
*Ca+2↑,
*Na+↑,
*UCPs↑, by increasing thermogenic gene expression such as uncoupling protein 1 (UCP-1), Sirtuin 1 (SIRT-1) [25] and peroxisome proliferator-activated receptor -γ (PPARγ) coactivator 1α (PGC-1α)
*SIRT1↑,
*PPARγ↑,
*Inflam↓, suppressing inflammatory responses, increasing lipid oxidation, inhibiting adipogenesis
*lipid-P↑,
*IL6↓, decreasing the expression of inflammatory biomarkers such as IL-6, TNF, and CCL-2, associated with NF-κB inactivation
*TNF-α↓,
*NF-kB↓,
*p‑Akt↑, Phosphorylation of Akt is also described after capsaicin treatment, which results in disruption of the NRF2/Keap complex and release of activated transcription factor NRF2
*NRF2↑,
*HO-1↑, triggers the transcription of heme-oxygenase1 genes, which are essential for heme degradation and prevention of oxidative damage
*ROS↑,
*GutMicro↑, It is suggested that regular treatment with capsaicin increases diversity in the gut microbiota and abundance of short-chain fatty acid (SCFA)-producing bacteria

5858-

CAP,

Capsaicin as a Microbiome Modulator: Metabolic Interactions and Implications for Host Health

Review,

Nor,

Review,

AD,

*BBB↓, crosses the blood–brain barrier, alters neurotransmitter levels, and accumulates in brain regions involved in cognition.
*GutMicro↑, capsaicin appears to undergo microbial transformation and influences gut microbial composition, favoring short-chain fatty acid producers and suppressing pro-inflammatory taxa. often favoring the growth of beneficial taxa such as Ruminococcaceae, Lac
Obesity↓, These changes contribute to anti-obesity, anti-inflammatory, and potentially anticancer effects
*Inflam↓,
*AntiCan↑,
*TRPV1↑, Capsaicin is a potent agonist perceived by TRPV1, a transmembrane cation channel that functions with Ca2+.
*Ca+2↑, causes an increase in Ca2+ flux,
*antiOx↑, Capsaicin is a bioactive compound of chili peppers responsible for their spicy flavor, which also shows antioxidant, anti-obesity, analgesic, anti-inflammatory, anticarcinogenic, and cardioprotective effects
*cardioP↑,
*BioAv↓, capsaicin exhibits low systemic bioavailability due to its rapid metabolism in the liver and other tissues, resulting in a short plasma half-life of approximately 25 min in humans
*Half-Life↓,
*BioAv↝, Capsaicin’s bioavailability is determined by multiple interrelated factors, including its physicochemical properties, metabolic transformations, route of administration, and the biological context of the host, including gut microbiota composition.
*BioAv↑, For instance, polymeric micelles, liposomes, and hydroxypropyl-β-cyclodextrin complexes have demonstrated the capacity to enhance capsaicin’s oral bioavailability, prolong its plasma half-life, and improve therapeutic consistency
*neuroP↑, capsaicin exposure alters glutamate, GABA, and serotonin levels in distinct brain regions, with potential implications for neuroprotection, mood regulation, and energy metabolism.
Apoptosis↑, apoptosis is the main mechanism by which capsaicin induces cell death in cancer cells.
p38↑, capsaicin triggers a calcium flux within the cell via TRPV1, activating the p38 pathway.
ROS↑, As a result, reactive oxygen species (ROS) are produced, along with depolarization of the mitochondrial membrane potential and opening of the mitochondrial permeability transition pore.
MMP↓,
MPT↑,
Cyt‑c↑, Consequently, cytochrome c is released, the apoptosome is assembled, and caspases are activated, ultimately leading to cell death
Casp↑,
TRIB3↑, capsaicin enhances TRIB3 gene expression, which allowed an increase in the antiproliferative and proapoptotic effects of TRIB3 in cancer cells
NADH↓, Capsaicin has also been seen to downregulate and inhibit tumor-associated NADH oxidase (tNOX) and Sirtuin1 (SIRT1) in multiple cancer cell lines such as bladder cancer, which led to reduced cell growth and migration
SIRT1↓,
TumCG↓,
TumCMig↓,
TOP1↓, pointing out that capsaicin had an inhibitory effect on topoisomerases I and II, causing a reduction in metabolic activity and proliferation of a human colon cancer cell line
TOP2↓,
β-catenin/ZEB1↓, with capsaicin, the β-catenin transcription gets downregulated
*ROS↓, Capsaicin has also been proven to alleviate redox imbalance or oxidative stress, thanks to its antioxidative activity.
*Aβ↓, Alsheimer’s disease, attenuating neurodegeneration in mice by reducing amyloid-beta levels via the promotion of non-amyloidogenic processing of amyloid precursor protein

5933-

CAR,

Protective Effect of Carvacrol against Gut Dysbiosis and Clostridium difficile Associated Disease in a Mouse Model

in-vivo,

IBD,

mice

*Diar↓, Carvacrol supplementation significantly reduced the incidence of diarrhea and improved the clinical and diarrhea scores in mice (p < 0.05).
*GutMicro↑, Microbiome analysis revealed a significant increase in Proteobacteria and reduction in the abundance of protective bacterial flora in antibiotic-treated and C.
*Dysb↓, Results suggest that CR could potentially be used to control gut dysbiosis and reduce C. difficile infection

5932-

CAR,

Carvacrol attenuates mucosal barrier impairment and tumorigenesis by regulating gut microbiome

in-vivo,

IBD,

Male C57BL/6 J mice

in-vivo,

Park,

*GutMicro↑, Carvacrol can regulate the gut microbiota. bundance of specific microbiota, such as Lactobacillus, Escherichia coli/Shigella, and Lachnoclostridium.
Risk↓, Carvacrol inhibits the development of colitis-associated colorectal cancer.
*Inflam↓, nti-inflammatory and antioxidant traits,
*antiOx↓,
*ZO-1↑, carvacrol significantly restored colonic length (p < 0.01) and re-established key tight junction proteins like ZO-1.
*iNOS↓, downregulated mRNA levels of inflammatory mediators such as iNOS and IL-6.
*IL6↓,
*NO↓, carvacrol has been shown to suppress nitric oxide and prostaglandin E2 production
*PGE2↓,
*memory↑, carvacrol improves memory deficits in Parkinson’s disease models
*TLR4↓, anti-inflammatory effects of carvacrol by inhibiting the TLR4/NF-κB signaling pathway
*NF-kB↓,
*IBI↑, Carvacrol improves intestinal barrier function
*CLDN3↑, expression levels of ZO-1, Claudin3, Claudin1, Occludin, and Mucin were significantly increased in the carvacrol group compared to the DSS group
*CLDN1↑,
*MUC1↑,
*OCLN↑,
*iNOS↑, carvacrol significantly inhibited the mRNA expression levels of iNOS, COX-2, Interferon-γ, IL-1β, and IL-6 in the intestinal tracts of colitis mice
*COX2↓,
*IFN-γ↓,
IL1β↓,
ADAM10?,

6022-

CGA,

Chlorogenic Acid: Recent Advances on Its Dual Role as a Food Additive and a Nutraceutical against Metabolic Syndrome

Review,

Nor,

*antiOx↑, including anti-oxidant, anti-inflammatory, antilipidemic, antidiabetic, and antihypertensive activities.
*Inflam↓,
*AntiDiabetic↑,
*Obesity↓, chlorogenic acid as a nutraceutical for the prevention and treatment of metabolic syndrome and associated disorders, including in vivo studies, clinical trials, and mechanisms of action
*Wound Healing↑, It was found that chlorogenic acid accelerated wound healing.
*BP↓, Significant reductions of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were observed
*Dose↝, A total of 23 healthy subjects (four men and 19 women) were given water (control) and 400 mg of chlorogenic acid dissolved in 200 mL of low nitrate water.
*ROS↓, the mechanism proposed was that chlorogenic acid scavenges reactive oxygen species (ROS) generated by consumption of high-fat diet, which suppresses the expression of inflammation, and consequently reduces fat accumulation,
*Fas↓, chlorogenic acid supplementation in high-fat diet-induced-obese mice significantly inhibited fatty acid synthase (FAS),
*HMG-CoA↓, As for hypercholesterolemia, chlorogenic acid has been found to inhibit 3-hydroxy-3-methylglutaryl CoA reductase (HMGCR)
*GutMicro↑, high-CGAs coffee (80.8 mg) induced a significant increase in the growth of Bifidobacterium spp. as well as Clostridium coccoides-Eubacterium rectale group, the latter group having also potential to benefit human health.

6016-

CGA,

Coffee Chlorogenic Acids Incorporation for Bioactivity Enhancement of Foods: A Review

Review,

Var,

Review,

AD,

Review,

Diabetic,

antiOx↑, CGAs have been associated with health benefits, such as antioxidant, antiviral, antibacterial, anticancer, and anti-inflammatory activity, and others that reduce the risk of cardiovascular diseases, type 2 diabetes, and Alzheimer’s disease.
*Bacteria↓,
AntiCan↑,
*Inflam↓,
*cardioP↑, reduce the risk of cardiovascular disease by suppressing the expression of P-selectin in platelets
*AntiDiabetic↑,
*GutMicro↑, non-absorbed part of 5-CQA and caffeic acid in the human gastrointestinal tract serves as a substrate for beneficial intestinal microbiota,
*eff↑, The fortification of foods with coffee CGAs has the potential to improve the functionality of foods.
*eff↑, exposing them to monopolar pulses of 2 Hz with an interval of 0.5 s and generating an electric field of 28 kV/10 cm with water at 20 °C. The use of an electric field increased radical scavenging activity up to 31% and 11%, for green and roasted coffe
*ROS↓, CGAs are known to exhibit a radical scavenging effect similar to ascorbic acid
*IronCh↑, CGAs can chelate transition metals such as Fe2+ to scavenge free radicals and disrupt chain reactions
*neuroP↑, The neuroprotective mechanisms of coffee are suggested to be related to the anti-inflammatory effects of caffeine and CGAs on A1 and A2 receptors.
*AChE↓, some coffee compounds could inhibit brain acetylcholinesterase and butyrylcholinesterase
*BChE↓,
*chemoPv↑, Several mechanisms have suggested that CGAs may have a chemopreventive effect
*BioAv⇅, the absorption and bioavailability of CGAs are controversial due to the significant interindividual differences regarding their utilization, metabolism, and excretion found in scientific and clinical studies

6011-

CGA,

Chlorogenic Acid’s Role in Metabolic Health: Mechanisms and Therapeutic Potential

Review,

Nor,

*BioAv↓, CGA’s oral bioavailability remains limited, prompting research into optimized extraction methods, novel formulations, and structural modifications.
*antiOx↑, antioxidant, anti-inflammatory, anticancer, antibacterial, hepatoprotective, cardioprotective and neuroprotective effects, and modulation of lipid and glucose metabolism
*Inflam↓,
*Bacteria↓,
*hepatoP↑,
*cardioP↑,
*neuroP↑,
*ROS↓, CGA action include inhibition of oxidative stress, regulation of inflammatory responses through modulation of the NF-κB pathway and activation of the Nrf2 pathway
*NF-kB↓, inhibition of NF-κB
*NRF2↑,
*Obesity↓, Research demonstrates that CGA may influence body weight regulation through multiple pathways, including modulation of gut microbiota, reduction of inflammation, regulation of adipogenesis, and stimulation of thermogenesis.
*GutMicro↑, increasing the abundance of probiotic bacteria such as Bifidobacterium and Lactobacillus, while reducing the abundance of bacterial strains found in obese patients and animals, such as Desulfovibrionaceae, Ruminococcaceae, Lachnospiraceae, and Erysip
*AntiAg↑, antiplatelet effects of CGA are supported by both in vitro and in vivo studies
*cardioP↑, CGA was recognized as a compound with high cardioprotective potential, considering its antioxidant, anti-inflammatory, and antihypertensive activities
*AntiDiabetic↑, CGA alleviates the effects of type 2 diabetes mellitus (DM) and helps prevent its development
*NLRP3↓, CGA also inhibits the NLRP3 inflammasome via Nrf2 activation, significantly decreasing proteinuria, creatinine, and urea levels in diabetic rats
*OCLN↓, figure 3
*VEGF↓,
BioAv↝, CGA is water-soluble but highly unstable when exposed to elevated temperature, light, oxygen, or alkaline pH

6045-

CGA,

SeNPs,

A Flower-like Brain Targeted Selenium Nanocluster Lowers the Chlorogenic Acid Dose for Ameliorating Cognitive Impairment in APP/PS1 Mice

in-vivo,

AD,

APP/PS1 Mice

*neuroP↑, Chlorogenic acid (CGA) is one of the most common dietary polyphenols with neuroprotective effects.
*BioAv↑, CGA were used to prepare a new flowerlike selenium nanocluster (TGN-CGA@SeNCs) for enhancing the bioavailability of CGA.
*GutMicro↑, At the same concentration, the CGA-modified selenium nanocluster (CGA@SeNCs) and TGN-CGA@SeNCs showed better function in ameliorating the gut microbiota disorder.
*BBB↑, Notably, only TGN-CGA@SeNCs can transport through the blood-brain barrier (BBB)
*Aβ↓, and TGN-CGA@SeNCs showed better effects than CGA@SeNCs in regulating Aβ aggregation and improving brain glucose homeostasis.
*glucose↝,

6023-

CGA,

Pharmacological advances of the chlorogenic acids family: current insights and future research directions

Review,

AD,

Review,

Park,

Review,

IBD,

*Aβ↓, chlorogenic acid can reduce Aβ plaques in Alzheimer’s disease model mice by 37%, indicating its neuroprotective potential.
*neuroP↑,
*cardioP↑, Similarly, CGAs offer protection to the cardiovascular system, gastrointestinal tract, kidneys, and liver, while additionally preventing metabolic syndrome and displaying anticancer and antimicrobial capabilities.
*GastroP↑,
*RenoP↑,
*hepatoP↑,
*Obesity↓,
*Bacteria↓,
*BioAv↑, hydroxycinnamoyl-CoA quinate hydroxycinnamoyl transferase, HQT in tomatoes significantly enhances CGA accumulation without significantly altering the levels of other soluble phenolic botanical drugs.
*BioAv↑, Mechanistic studies have shown that dietary fats (such as soybean oil and coconut oil) can significantly enhance the permeability of CGA in the Caco-2 monolayer by increasing cell membrane fluidity
*BioAv↑, Following oral administration of CGA, the acidic environment in the stomach helps maintain the structural stability of CGA, with approximately one-third of the dose entering the blood system through passive diffusion in the small intestine, while the
*ROS↓, CGA pretreatment markedly diminished ROS caused by PD toxins
*GutMicro↑, CGA works with the gut microbiota and its metabolites to alleviate post-infectious irritable bowel syndrome (PI-IBS)
*IBI↑, CGA increases intestinal damage repair, decreases MCT-1 and TFF-3 expression, and suppresses NF-κB expression
*MCT1↓,
*NF-kB↓,
*DNMT1↓, Liver Cancer, DNMT1 protein expression↓

4487-

Chit,

PreB,

Unravelling the Role of Chitin and Chitosan in Prebiotic Activity and Correlation With Cancer: A Narrative Review

Review,

NA,

*GutMicro↑, As a nondigestible dietary fiber, chitin falls into the category of a prebiotic
Apoptosis↑, Chitosan Involvement in Apoptosis and Cytotoxicity in Cancer Cells
BAX↑, chitosan was shown to upregulate the pro-apoptotic protein Bax and downregulate the anti-apoptotic Bcl-2
Bcl-2↓,
*Inflam↓, in vitro and in vivo studies to consistently demonstrate anti-inflammatory and antitumor activities
AntiTum↑,

6079-

CHL,

Chlorophyllin Modulates Gut Microbiota and Inhibits Intestinal Inflammation to Ameliorate Hepatic Fibrosis in Mice

in-vivo,

Nor,

mice

*eff↑, oral administration of chlorophyllin could attenuate intestinal and hepatic inflammation and ameliorate liver fibrosis.
*GutMicro↑, oral administration of chlorophyllin promptly rebalanced the gut microbiota, exhibiting down-regulation of the phylum Firmicutes and up-regulation of the phylum Bacteroidetes.
*NF-kB↓, chlorophyllin exposure could inhibit NF-κB pathway via IKK-phosphorylation suppression.
*MMPs↑, Chlorophyllin Treatment Increased the MMP/TIMP Ratio, Which May Promote Fibrolysis and Resolving Liver Fibrosis
*TIMP1↓,
*Inflam↓, Exposure of Intestinal Epithelial Cells With Chlorophyllin Can Attenuate Inflammatory Signaling Pathways
*Dysb↓, Dysbiosis Occurring in Liver Fibrosis Can Be Rebalanced by Oral Administration of Chlorophyllin for Eubiosis

Showing Research Papers: 1 to 50 of 115
Page 1 of 3 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 115

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

CD8+↑, 2,
Total Targets: 159

Pathway results for Effect on Normal Cells:

NA, unassigned ⓘ

Dysb↓, 2,

Redox & Oxidative Stress ⓘ

antiOx↓, 2, antiOx↑, 11, Catalase↑, 2, GPx↑, 2, GSH↑, 3, GSTs↑, 1, HDL↑, 1, HO-1↑, 1, Keap1↓, 1, lipid-P↓, 2, lipid-P↑, 1, MDA↓, 2, MPO↓, 2, NRF2↑, 4, ROS?, 1, ROS↓, 14, ROS↑, 1, ROS↝, 1, SOD↑, 5, TBARS↓, 1, UCPs↑, 1, VitC↑, 1,

Metal & Cofactor Biology ⓘ

IronCh↑, 2,

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,

Core Metabolism/Glycolysis ⓘ

adiP↓, 1, ALAT↓, 1, glucose↝, 1, H2S↑, 1, HMG-CoA↓, 1, LDH↓, 2, LDL↓, 1, PPARγ↑, 1, SIRT1↑, 1,

Cell Death ⓘ

Akt↓, 1, p‑Akt↑, 1, Apoptosis↑, 1, DR4↓, 1, Fas↓, 1, iNOS↓, 3, iNOS↑, 1, p‑JNK↓, 1, MCT1↓, 1, p38↓, 1, TRPV1↑, 2,

Transcription & Epigenetics ⓘ

other↓, 1, other↑, 3,

DNA Damage & Repair ⓘ

DNAdam↓, 1, DNMT1↓, 1, P53↓, 1, RAD51↓, 1,

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1, STAT3↓, 1,

Migration ⓘ

5LO↓, 2, AntiAg↑, 2, Ca+2↑, 2, CLDN1↑, 1, MMP2↓, 1, MMP3↓, 1, MMP9↓, 1, MMPs↑, 1, MUC1↑, 1, Na+↑, 1, TIMP1↓, 1, ZO-1↑, 2,

Angiogenesis & Vasculature ⓘ

NO↓, 4, NO↑, 1, VEGF↓, 1,

Barriers & Transport ⓘ

BBB↓, 1, BBB↑, 4, CLDN3↑, 1, GastroP↑, 1, IBI↑, 2, Na+↑, 1, OCLN↓, 1, OCLN↑, 1,

Immune & Inflammatory Signaling ⓘ

COX1↓, 1, COX2↓, 5, CRP↓, 1, IFN-γ↓, 1, IFN-γ↑, 1, IL10↑, 4, IL17↓, 1, IL17↑, 1, IL1β↓, 4, IL6↓, 7, IL6↑, 1, Imm↑, 2, Inflam↓, 20, NF-kB↓, 10, PGE2↓, 4, PGE2↑, 1, Th1 response↓, 1, Th2↑, 2, TLR4↓, 1, TNF-α↓, 7,

Synaptic & Neurotransmission ⓘ

5HT↑, 1, AChE↓, 1, BChE↓, 1, BDNF↑, 1,

Protein Aggregation ⓘ

Aβ↓, 3, NLRP3↓, 1, β-Amyloid↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 4, BioAv↑, 6, BioAv⇅, 1, BioAv↝, 4, Dose↝, 2, eff↓, 4, eff↑, 7, eff↝, 2, Half-Life↓, 2, Half-Life↑, 1, Half-Life↝, 1,

Clinical Biomarkers ⓘ

ALAT↓, 1, AST↓, 1, BP↓, 3, creat↓, 1, CRP↓, 1, GutMicro↑, 26, IL6↓, 7, IL6↑, 1, LDH↓, 2,

Functional Outcomes ⓘ

AntiAge↑, 1, AntiCan↑, 2, AntiDiabetic↑, 4, BOLD↑, 1, cardioP↓, 1, cardioP↑, 9, chemoP↑, 1, chemoPv↑, 1, cognitive↑, 3, hepatoP↑, 5, memory↑, 4, motorD↑, 1, neuroP↑, 11, Obesity↓, 3, radioP↑, 1, RenoP↑, 1, Risk↓, 5, toxicity↓, 2, Weight↓, 2, Wound Healing↑, 2,

Infection & Microbiome ⓘ

Bacteria↓, 4, Diar↓, 1,
Total Targets: 145

Scientific Paper Hit Count for: GutMicro, Gut Microbiota

8 Butyrate
8 Selenium NanoParticles
7 immunotherapy
6 Urolithin
5 Chlorogenic acid
4 Akkermansia
4 Bifidobacterium
4 diet FMD Fasting Mimicking Diet
4 Rosmarinic acid
4 Selenite (Sodium)
3 Allicin (mainly Garlic)
3 beta-glucans
3 Berberine
3 probiotics
3 Carvacrol
3 Ferulic acid
3 Hydrogen Gas
3 Pterostilbene
2 Anthocyanins
2 Astaxanthin
2 Baicalein
2 Vitamin B3,Niacin
2 Capsaicin
2 chitosan
2 Curcumin
2 Chemotherapy
2 Luteolin
2 Phenylbutyrate
2 Resveratrol
2 Taurine
2 Thymol-Thymus vulgaris
1 5-Hydroxytryptophan
1 Alpha-Lipoic-Acid
1 Aspirin -acetylsalicylic acid
1 Atorvastatin
1 Aloe anthraquinones
1 Radiotherapy/Radiation
1 Baicalin
1 Boron
1 Boswellia (frankincense)
1 Bruteridin(bergamot juice)
1 Paclitaxel
1 Prebiotic
1 Chlorophyllin
1 Chocolate
1 Cinnamon
1 Calorie Restriction Mimetics
1 diet Methionine-Restricted Diet
1 Fucoidan
1 Shilajit/Fulvic Acid
1 Gallic acid
1 Lecithin
1 Lycopene
1 Magnolol
1 Magnetic Fields
1 nicotinamide adenine dinucleotide
1 Naringin
1 Quercetin
1 Sulforaphane (mainly Broccoli)
1 Silymarin (Milk Thistle) silibinin
1 Shikonin
1 Aflavin-3,3′-digallate
1 Ursolic acid
1 Vitamin D3

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#:350  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

GutMicro Cancer Research Results

Pathway results for Effect on Cancer / Diseased 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 ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned ⓘ

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

DNA Damage & Repair ⓘ

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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