Imm Cancer Research Results
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Enhance the immune response in patients.
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Scientific Papers found: Click to Expand⟱
other↝, Since the use of ALA-based drugs for tumor diagnosis or therapy depends on preferential PpIX tumor accumulation, we begin this review with an overview of PpIX biosynthesis from ALA and end with the prospect of combining the diagnostic and therapeutic
ROS↑, These components individually are not harmful but become cytotoxic when combined due to the generation of reactive oxygen species (ROS) via type I and II photochemical reactions.
other↝, ALA was known to cause endogenous PpIX accumulation in human lymphocytes in the 1970s [15].
mtDam↑, which causes direct mitochondrial structural damage and Ca2+ release [24].
Ca+2↑,
ER Stress↑, ALA-PDT is known to damage the endoplasmic reticulum (ER) and cause Ca2+ release, triggering apoptosis through ER-stress signaling [25].
Apoptosis↑,
TumAuto↑, Lastly, ALA-PDT is also known to induce autophagy, the degradation of cellular components by lysosomes.
other↝, ALA administration exhibits red fluorescence and photosensitizing activity upon light activation.
Dose↝, Although blue and red light-emitting diode (LED) illuminators are commonly used as the light source to activate ALA and MAL for PDT of AK lesions, natural daylight is emerging as an attractive and convenient alternative.
Imm↑, ALA-PDT not only directly kills tumor cells but also elicits potent immune responses with important implications in the long-term therapeutic outcome.
*Imm↑, AR possesses various biological functions, including potent immunomodulation, antioxidant, anti-inflammation and antitumor
activities.
*antiOx↑,
*Inflam↓,
AntiTum↑,
eff↑, characteristics of increasing curative effect and reducing the toxicity of chemotherapeutic drugs [11 , 118].
chemoP↑,
Dose↝, main bioactive compounds responsible for the anti-cancer effects of AR mainly include formononetin,
AS-IV and APS. S
TumCMig↓, AS-IV could inhibit the migration and proliferation of non-small cell lung cancer (NSCLC
TumCP↓,
Akt↓, h via inhibition of the Akt/GSK-3β/β-catenin
signaling axis.
GSK‐3β↓,
MMP2↓, downregulating the expression of matrix metalloproteases (MMP)-2 and -9
MMP9↓,
EMT↓, AS-IV could inhibit TGF-B1 induced EMT through inhibition of PI3K/AKT/NF-KB
PI3K↓,
Akt↓,
NF-kB↓,
Inflam↓,
TGF-β1↓,
TNF-α↓,
IL6↓,
Fas↓, reduced FAS/FasL
FasL↓,
NOTCH1↓, decressing notch1
JNK↓, inactivating JNK pathway [145]
TumCG↓, The results showed that the AR water extract could inhibit the growth of colorectal cancer in vivo without apparent toxicity and side effect, which suggests that AR is a potential therapeutic drug for colorectal cancer
AntiTum↑, APS has been increasingly used in cancer therapy owing to its anti-tumor ability as it prevents the progression of prostate, liver, cervical, ovarian, and non-small-cell lung cancer by suppressing tumor cell growth and invasion and enhancing apoptosi
TumCG↓,
TumCI↓,
Apoptosis↑, after APS treatment, the apoptosis of HepG2 cells is accelerated (57).
Imm↑, APS enhances the sensitivity of tumors to antineoplastic agents and improves the body’s immunity
Bcl-2↓, Huang et al. proposed that APS induces H22 (a hepatocellular cancer [HCC] cell line) apoptosis by downregulating Bcl-2 and upregulating Bax expression (56).
BAX↑,
Wnt↓, downregulating the Wnt/β-catenin signaling pathway.
β-catenin/ZEB1↓,
TumCG↓, APS effectively inhibited the growth of MDA-MB-231 (a human breast cancer [BC] cell line) graft tumor (58)
miR-133a-3p↑, apoptosis rate of human osteosarcoma MG63 cells increased owing to the upregulation of miR-133a and inactivation of the JNK signaling pathways (71).
JNK↓,
Fas↑, Li and Shen found that APS can induce apoptosis by activating the Fas death receptor pathway.
P53↑, Zhang et al. showed that APS could activate p53 and p21 and inhibit the expression of Notch1 and Notch3 in vitro, ultimately inhibiting cell proliferation and promoting their apoptosis
P21↑,
NOTCH1↓,
NOTCH3↓,
TumCP↓,
TumCCA↑, Liu et al. found that APS induced the cell cycle of bladder cancer UM-UC-3 to stop in the G0/G1 phase, thus inhibiting its proliferation
GPx4↓, APS was found to reduce GPX4 expression, inhibit the activity of the light chain subunit SLC7A11 (xCT), and promote the formation of BECN1-xCT complex by activating AMPK/BECN1 signaling.
xCT↓,
AMPK↑,
Beclin-1↑,
NF-kB↓, APS could control the proliferation of lung cancer cells (A549 and NCI-H358 cells) by inhibiting the NF-κB signaling pathway (97)
EMT↓, APS treatment led to reduced EMT markers (vimentin, AXL) and MIF levels in cells.
Vim↓,
TumMeta↓, APS inhibits Lewis lung cancer growth and metastasis in mice by significantly reducing VEGF and EGFR expression in cancerous tissues
VEGF↓,
EGFR↓,
eff↑, Nano-drug delivery systems can increase efficiency and reduce toxicity
eff↑, Jiao et al. developed selenium nanoparticles modified with macromolecular weight APS and observed positive results in hepatoma treatment
MMP↓, Subsequent investigations revealed that APS can decrease the ΔΨm values and Bcl-2, p-PI3K, P-gp, and p-AKT levels while elevating Bax expression.
P-gp↓,
MMP9↓, downregulation of MMP-9 expression,
ChemoSen↑, Li et al. observed that APS could enhance the sensitivity of SKOV3 ovarian cancer cells to CDDP treatment by activating the mitochondrial apoptosis pathway and JNK1/2 signaling pathway
SIRT1↓, APS significantly suppressed SIRT1 and SREBP1 expression, decreased cholesterol and triglyceride levels in PC3 and DU145, and attenuated cell proliferation.
SREBP1↓,
TumAuto↑, APS can induce autophagy in colorectal cancer cells by inhibiting the PI3K/AKT/mTOR axis and the development of cancer cells.
PI3K↓,
mTOR↓,
Casp3↑, Shen found that APS elevated caspase-9, caspase-3, and Bax protein levels, decreased Bcl-2 protein expression, and inhibited CD133 and CD44 co-positive colon cancer stem cell proliferation time
Casp9↑,
CD133↓,
CD44↓,
CSCs↓,
QoL↑, QOL was significantly improved as indicated by the reduction in pain and improvement in appetite
ChemoSen↑, review aims to determine the clinical efficacy and safety of Astragalus Polysaccharide Injection (APS) combined with chemoradiotherapy for cervical cancer based on existing data.
eff↑, APS combined with chemoradiotherapy improved the objective response rate (ORR, RR = 1.43, 95% CI: 1.24–1.64) and disease control rate (
RadioS↑, APS can enhance the clinical efficacy of radiotherapy and chemotherapy for cervical cancer, respectively.
CEA↓, APS further reduced tumor marker levels: CEA (MD = −1.24, 95% CI: −1.58 to −0.89, p < 0.00001; heterogeneity: χ2 = 1.75, p = 0.19, I2 = 43%), SCC (
Wnt↓, Specifically, APS inhibits the cisplatin resistance pathway and regulates the cell cycle by suppressing the Wnt/β-catenin pathway via the PPARD/CDC20 axis (Liu et al., 2025)
β-catenin/ZEB1↓,
γH2AX↑, APS also influences autophagy and upregulates γH2AX expression, thereby enhancing cervical cancer sensitivity to radiotherapy
ER Stress↑, APS alleviates endoplasmic reticulum stress and promotes mitochondrial autophagy, thereby enhancing apoptosis and mitigating cisplatin-induced toxicity
mt-TumAuto↑,
QoL↑, suggested that APS combination therapy improves short-term clinical efficacy, quality of life, and immune function
Imm↑,
AntiCan↑, Preclinical studies indicate that APS exerts significant anti-liver cancer effects through multiple biological actions, including the promotion of apoptosis, inhibition of proliferation, suppression of epithelial–mesenchymal transition, regulation of
Apoptosis↑,
TumCP↓,
EMT↓,
Imm↑, improving host immune response
ChemoSen↑, APS exhibits synergistic effects when combined with conventional chemotherapeutics and interventional treatments such as transarterial chemoembolisation, improving efficacy and reducing toxicity.
BioAv↓, limitations such as low bioavailability and a lack of large-scale clinical trials remain challenges for clinical translation.
TumCG↓, APS significantly inhibited tumour growth in H22-bearing mice with a dose-dependent effect (100, 200, 400 mg/kg), with the 400 mg/kg group achieving a tumour inhibition rate of 59.01%
IL2↑, APS enhance the thymus and spleen indices and elevates the key cytokines, including IL-2, IL-12, and TNF-α.
IL12↑,
TNF-α↑,
P-gp↓, APS reversed chemoresistance by downregulating P-glycoprotein and MDR1 mRNA expression
MDR1↓,
QoL↑, These effects contributed to improved treatment tolerance and enhanced quality of life [39].
Casp↑, APS can activate both the intrinsic and extrinsic apoptotic pathways, leading to caspase activation and DNA fragmentation
DNAdam↑,
Bcl-2↓, Mechanistically, APS downregulate antiapoptotic proteins such as Bcl-2 while upregulating proapoptotic proteins such as Bax and cleaved caspase-3.
BAX↑,
MMP↓, APS have been shown to disrupt the mitochondrial membrane potential and promote the release of cytochrome c, thereby enhancing apoptotic cascades in hepatocellular carcinoma models.
Cyt‑c↑,
NOTCH1↓, APS (0.1, 0.5, and 1.0 mg/mL) were shown to reduce both mRNA and protein levels of Notch1 in a concentration-dependent manner.
GSK‐3β↓, APS significantly inhibited the proliferation of HepG2 cells by downregulating the expression of glycogen synthase kinase-3β (GSK-3β), with 200 μg/mL being the most effective concentration.
TumCCA↑, APS exerted these effects by inducing cell cycle arrest at the G2/M and S phases, thereby impeding tumour cell proliferation [35].
GSH↓, HepG2 cells. APS also reduced intracellular glutathione (GSH) levels, increased reactive oxygen species (ROS) and lipid peroxidation levels, and elevated intracellular iron ion concentrations—all in a dose-dependent manner.
ROS↑,
lipid-P↑,
c-Iron↑,
GPx4↓, APS treatment led to the downregulation of GPX4 and upregulation of ACSL4, indicating that APS promotes ferroptosis in liver cancer cells.
ACSL4↑,
Ferroptosis↑,
Wnt↓, inhibit the expression of key proteins involved in the Wnt/β-catenin signalling pathway
β-catenin/ZEB1↓,
cycD1/CCND1↓, by downregulating the key oncogenic targets, including β-catenin, C-myc, and cyclin D1, which subsequently reduces Bcl-2 expression and activates the apoptotic cascade in HepG2 liver cancer cells.
Akt↓, It also inhibited the Akt/p-Akt signalling pathway.
PI3K↓, APS inhibit the PI3K/AKT/mTOR signalling pathway, which is a central negative regulator of autophagy.
mTOR↓,
CXCR4↓, PS upregulated the epithelial marker E-cadherin while downregulating the mesenchymal marker vimentin and the chemokine receptor CXCR4 at both mRNA and protein levels, suggesting that APS suppress liver cancer cell growth and metastasis by inhibiting
Vim↓,
PD-L1↓, APS interfere with immune checkpoint signalling by downregulating Programmed death-ligand 1 (PD-L1) expression on tumour cells.
eff↑, The preparation of polysaccharide–SeNP composites typically involves using sodium selenite (Na2SeO3) as the precursor and ascorbic acid (Vc) as the reducing agent, with synthesis carried out via a chemical reduction method in a polysaccharide solutio
eff↑, Mechanistic investigations revealed that AASP–SeNPs elevated intracellular ROS levels and reduced the mitochondrial membrane potential (∆Ψm).
ChemoSen↑, APS enhance doxorubicin-induced endoplasmic reticulum (ER) stress by reducing O-GlcNAcylation levels, thereby promoting apoptosis of liver cancer cells.
ChemoSen↑, APS inhibited BEL-7404 human liver cancer cell growth in a concentration-dependent manner and showed stronger cytotoxicity when combined with cisplatin.
chemoP↑, APS protects against chemotherapy-induced liver injury, particularly that caused by CTX, through antiapoptotic mechanisms
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.
Apoptosis↑, Astaxanthin causes apoptosis in
several in vitro studies, including both oral and liver cancer cells
EMT↓, AXT inhibits the EMT pathway in colon cancer cells and can reduce breast cancer cells' proliferation and growth
AntiCan↑, Astaxanthin can address human health problems, including cancer, cardiovascular, and neurodegenerative diseases.
*cardioP↑,
*neuroP↑,
TumCG↓, 100 mg/kg Astaxanthin strongly inhibited tumor growth relative to the TC group, with an inhibitory rate of 41.7%.
*antiOx↑, .ASX is often referred to as the "super antioxidant" since it has the strongest antioxidant activity of current carotenoids.
*Bacteria↓, Studies have demonstrated antioxidant and antimicrobial, immunomodulatory, hepatoprotective, anticancer, and antidiabetic effects of ASX.
*Imm↑,
*hepatoP↑,
*AntiDiabetic↑,
ROS↓, Astaxanthin and carbendazim function in conjunction to inhibit cell proliferation while reducing ROS production in
breast cancer cells.
*chemoPv↑, Chemopreventive and therapeutic efficacy of astaxanthin against cancer
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*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].
*eff↑, In the results, found that the A. vera polysaccharides harvested during the rainy season stimulated the phagocytic activity with greater intensity than dry season and improvement NO and IL-6 production.
*IL6↑,
*toxicity↓, No cytotoxic effect was found on cell viability and they cause a significant proliferative effect on macrophages in a concentration-dependent manner.
*Imm↑, A. vera polysaccharides harvested during the rainy season possessed a stronger immunostimulatory effect compared to the extracts from leaves obtained during dry seasons
Imm↑, β-glucans have been shown to exert immunostimulatory effects in vitro and in vivo in experimental animal models.
*Dose↝, Subjects were randomized to either the β -glucan (n = 10) or the control group (n = 5). Subjects in the β-glucan group ingested β-glucan 1000 mg once daily for 7 days.
*BioAv↓, β-glucan was barely detectable in serum of volunteers at all time-points.
*toxicity↑, Oral β-glucan is inexpensive and well-tolerated, and therefore may represent a promising immunostimulatory compound for human use.
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.
Imm↑, β-glucan and its signaling pathway will undoubtedly open a new research area on its potential therapeutic applications, including as immunostimulants for antifungal and anti-cancer regimens.
BioAv↝, Despite their high molecular weight, β-glucans, when orally administered, are absorbed in the intestine and activate innate and adaptive immunities.
eff↑, It has been reported that a higher degree of structural complexity in β-glucans is associated with more potent immunomodulatory and anti-cancer effects. higher molecular weight (over than 450 kDa) glucan was more potent than lower molecular weight
AntiCan↑,
Dectin1↝, This review will depict in detail how the physicochemical nature of β-glucan contributes to its immunostimulating effect in hosts and the potential uses of β-glucan by elucidating the dectin-1 signal transduction pathway.
Dose↝, Orally administered, natural β-glucans, such as lentinan and schizophyllan, are known for showing their immunopotentiating effects, and have been used in tumor immunotherapy for more than 30 years.
BioAv↓, β-Glucans are too large to be absorbed in the small intestines.
Imm↑, Here, we show that β-glucan–induced trained immunity overcomes these barriers by reprogramming macrophages through H3K4me3-dependent epigenetic modifications and metabolic rewiring.
TNF-α↓, Beta-glucans suppress pro-inflammatory cytokines (e.g., TNF-α, IL-6) and tumor-promoting pathways like NF-κB, while modulating T-regulatory cells (Tregs) and downregulating PD-L1 to overcome immune evasion.
IL6↓,
NF-kB↓,
PD-L1↓,
Imm↑,
BAX↑, They induce apoptosis via Bax/Bcl-2 regulation, arrest cell cycles at G1/S or G2/M phases, and inhibit angiogenesis by targeting VEGF and MMPs.
Bcl-2↓,
TumCCA↑,
angioG↓,
VEGF↓,
MMPs↓,
OS↑, improved overall survival (OS) in melanoma (hazard ratio
chemoP↑, alongside reduced chemotherapy toxicity
eff↑, Synergy with PD-1/PD-L1 inhibitors enhances immunotherapy efficacy, particularly in immunogenic tumors.
BioAv↑, Advanced nano-delivery systems, including micelles and exosomes, improve bioavailability and tumor targeting.
Imm↑, One of the most well-studied trained immunity inducers, β-glucan, has been shown to reprogram HSPCs in the bone marrow,
ROS↑, Trained neutrophils induced by β-glucan exhibit enhanced degranulation and increased production of reactive oxygen species, enabling direct tumor cell killing (Kalafati et al., 2020).
Apoptosis↑, orally administered yeast-derived particulate β-glucan treatment reduces tumor burden and decreases the accumulation of PMN-MDSC, while simultaneously inducing oxidative burst and apoptosis in these cells
OS↑, In metastatic breast cancer models, trained immunity induced by particulate β-glucan has been shown to significantly prolong survival and reduce lung metastases
TumMeta↓,
Dose↝, Currently, i.p. injection of β-glucan is considered the gold standard in preclinical studies, as it induces robust trained immunity in mice.
Imm↑, The small β-glucans fragments are eventually released by the macrophages and taken up by other immune cells leading to various immune responses.
*BioAv↓, Repeated measurements of β-glucans in serum, however, revealed no systemic absorption of the agent following the oral administration. Nonetheless, the immunoglobulin A concentration in saliva increased significantly for the 400 mg/day arm, suggesting
OS↑, In a randomized trial, SPG combined with conventional chemotherapy improved the long term survival rate of patients with ovarian cancer [72].
ChemoSen↑, Maitake D-Fraction extracted from Grifola frondosa (Maitake mushroom) was found to decrease the size of the lung, liver and breast tumors in >60% of patients when it was combined with chemotherapy in a 2 arms control study comparing with chemotherapy
*Dectin1↑, we analyzed β-glucan-mediated Dectin-1 activation.
*Imm↑, this study, adds on to the existing in vitro model by specifically investigating macrophage responses and can be applied to select non-digestible dietary polysaccharides and other components for their potential to induce trained immunity
*TNF-α↓, OatβG even showed a reduction in TNF-α release compared to medium control.
*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.
Imm↑, Based on in vitro studies, β-glucans act on several immune receptors including Dectin-1, complement receptor (CR3) and TLR-2/6 and trigger a group of immune cells including macrophages, neutrophils, monocytes, natural killer cells and dendritic cells
*toxicity↓, β-glucans of different doses (100 mg/day, 200 mg/day or 400 mg/day) were given respectively for 4 consecutive days. No drug-related adverse events were observed.
eff↑, In general, bigger size and more complex β-glucans such as those derived from Ganoderma lucidum have higher immunomodulating potency.
Imm↑, It was found that despite a relatively low initial white cell count, oral β-glucan can stimulate proliferation and activation of peripheral blood monocytes in patients with advanced breast cancer.
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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].
*toxicity↓, It was observed that the administration of β-glucan is safe and well-tolerated.
Imm↑, concomitant administration of β-glucan with chemo or radiotherapy reduced the immune depression caused by such treatments and/or accelerated the recovery of white blood cells counts.
radioP↑,
chemoP↑,
PD-L1↓, lentinan treatment inhibited the platinum drug-stimulated expression of PD-L1 in gastric cancer cells mainly by suppressing MAPK signaling
MAPK↓,
OS↑, Lentinan has been reported to improve the overall survival of cancer patients receiving chemotherapy [23, 24] through its antitumor and immunomodulatory activitie
AntiTum↑,
Imm↑,
VEGF↓, VEGF-targeted agents to treat cancer patients by disrupting the tumor blood vessel supply. Of them, bevacizumab, an FDA-approved humanized monoclonal antibody against VEGF, is the most promising.
Imm↑, by anti-VEGF approaches affect the influx and activation of immune cells into tumors, which might influence the therapeutic results.
eff↑, outline the therapeutic potential of combining bevacizumab with other immune-stimulatory agents.
eff↑, Bifidobacterium bifidum was abundant in patients responsive to therapy.
Imm↑, only specific B. bifidum strains reduced tumour burden synergistically with PD-1 blockade or oxaliplatin treatment by eliciting an antitumour host immune response.
IFN-γ↑, In mice, these strains induced tuning of the immunological background by potentiating the production of interferon-γ, probably through the enhanced biosynthesis of immune-stimulating molecules and metabolites.
*Inflam↓, it should be mentioned that Bifidobacterium has a known anti-inflammatory role, mediated by the production of SCFAs and induction of Treg cells and IL-10, so it is not entirely unreasonable to doubt its ability to promote antitumor immune responses.
*Treg lymp↑,
*IL10?,
Imm↑, With specific regard to cancer, the intake of Bifidobacterium spp. conferred protection against CRC development in mice[77] and improved immune function in CRC patients[78].
eff↑, several works have linked Bifidobacterium to improved response to immunochemotherapy
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,
*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
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ROS↑, modulation of reactive oxygen species (ROS) formation and the resulting endoplasmic reticulum stress is central to BA’s molecular and cellular anticancer activities
ER Stress↑,
TumCG↓, Cell cycle arrest, growth inhibition, apoptosis induction, and control of inflammation are all the effects of BA’s altered gene expression
Apoptosis↑,
Inflam↓,
ChemoSen↑, BA has additional synergistic effects, increasing both the sensitivity and cytotoxicity of doxorubicin and cisplatin
Casp↑, BA decreases viability and induces apoptosis by activat-
ing the caspase-dependent pathway in human pancreatic
cancer (PC) cell lines
ERK↓, BA might inhibit the activation of Ak strain transforming (Akt) and extracellular signal–regulated kinase (ERK)1/2,
cl‑PARP↑, initiation of cleavage of PARP were prompted by the treatment with AKBA
AR↓, AKBA affects the androgen receptor by reducing its expression,
cycD1/CCND1↓, decrease in cyclin D1, which inhibits cellular proliferation
VEGFR2↓, In prostate cancer, the downregulation of vascular endothelial growth factor receptor 2–mediated angiogenesis caused by BA
CXCR4↓, Figure 6
radioP↑,
NF-kB↓,
VEGF↓,
P21↑,
Wnt↓,
β-catenin/ZEB1↓,
Cyt‑c↑,
MMP2↓,
MMP1↓,
MMP9↓,
PI3K↓,
MAPK↓,
JNK↑,
*5LO↓, Table 1 (non cancer)
*NRF2↑,
*HO-1↑,
*MDA↓,
*SOD↑,
*hepatoP↑, Preclinical studies demonstrated hepatoprotective impact for BA against different models of hepatotoxicity via tackling oxidative stress, and inflammatory and apoptotic indices
*ALAT↓,
*AST↓,
*LDH↑,
*CRP↓,
*COX2↓,
*GSH↑,
*ROS↓,
*Imm↑, oral administration of biopolymeric fraction (BOS 200) from B. serrata in mice led to immunostimulatory effects
*Dose↝, BA at low concentration tend to stimulate an immune response, as those utilized in the study of Beghelli et al. (2017) however, utilizing higher concentration suppressed the immune response
*eff↑, Useful actions on skin and psoriasis
*neuroP↑, AKBA has substantially diminished the levels of inflammatory markers such as 5-LOX, TNF-, IL-6, and meliorated cognition in lipopolysaccharide-induced neuroinflammation rodent models
*cognitive↑,
*IL6↓,
*TNF-α↓,
ROS↑, BP nanomaterials are capable of producing singlet oxygen, which enable its application as a photosensitizer for photodynamic therapy (PDT).
Imm↑, Recently, it has been reported that BP-based PTT is capable of activating immune responses and alleviating the immunosuppressive tumor microenvironment
PhotoS↑, BP nanomaterials can be applied as photothermal agents (PTA
*Imm↑, traditional uses that include improving immune response and cardiovascular function.
*cardioP↑,
*LDL↓, Multiple clinical trials have provided evidence that different forms of orally administered bergamot can reduce total cholesterol and low-density lipoprotein cholesterol.
toxicity↓, The use of bergamot in multiple clinical trials has consistently shown that it is well tolerated in studies ranging from 30 days to 12 weeks.
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);
*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
*Imm↑, CA enhances immune responses, reduces inflammation, exerts antimicrobial effects, and improves overall fish health.
*Inflam↓,
*Bacteria↓,
*eff↑, sustainable functional-feed strategies that diminish antibiotic reliance in aquaculture.
*ROS↓, Reduced MDA levels and ROS accumulation
*MDA↓,
*Catalase↑, Increased CAT, GSH, and T-AOC activities
*GSH↑,
*TAC↑,
*NF-kB↓, Suppressed the activation of the NF-κB signaling pathway and the NLRP3 inflammasome pathway in the gills
*NLRP3↓,
*eff↑, In rainbow trout (Oncorhynchus mykiss), co-supplementation with 1–3 g RA/kg and Lactobacillus rhamnosus yielded synergistic improvements in growth, antioxidant capacity, and stress tolerance
*AST↓, In rainbow trout, CinA (0.25–1.5 g/kg) lowered intestinal pH, serum triglycerides, and hepatic enzyme levels (AST and ALT), while upregulating hepatic antioxidant genes (SOD and GST) [49]
*ALAT↓,
*SOD↑,
*GSTA1↑,
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STAT3↓, Capsaicin induced an apoptotic cell death in PEL cells correlated with the inhibition of STAT3
Imm↑, Capsaicin has been reported to have also immune-modulating properties, being able to activate DCs through the vanilloid receptor 1 (VR1) [21]
*Bacteria↓, properties including anti-viral, anti-bacterial, anti-cancer, immunomodulatory, and wound-healing activities.
*AntiCan↑,
*Imm↑,
*Wound Healing↑,
*NF-kB↓, including inhibition of the transcription factors NF-κB
*5LO↓, use of CAPE in diabetes therapy have shown that caffeic acid phenethyl ester inhibits the enzyme 5-lipoxygenase
*AntiDiabetic↑, Antidiabetic Properties
ChemoSen↑, CAPE treatment enhances the antitumor effect of cytostatic drugs, such as vinblastine, paclitacol, estramustine and docetaxel, used in the chemotherapy of prostate cancer [76,81,82].
selectivity↑, CAPE acts selectively on diseased cells, without adversely affecting normal cells [88]
chemoPv↑, CAPE may be useful as support for cancer therapy in terms of chemoprevention of non-cancerous cells
*NF-kB↓, Our results show that the activation of NF-kappa B by tumor necrosis factor (TNF) is completely blocked by CAPE in a dose- and time-dependent manner.
*Imm↑, inhibitor of NF-kappa B activation and this may provide the molecular basis for its multiple immunomodulatory and antiinflammatory activities
*Inflam↓,
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*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↓,
*DNAdam↓, Uncaria tomentosa reduced the neutropenia caused by chemotherapy and was also able to restore cellular DNA damage.
Neut↓, A greater reduction in the white blood cell (WBCs) and the neutrophil counts were observed in the Ca group along the treatment, differently from the UtCa group, which remained closely the reference values
eff↑, We concluded that Ut is an effective adjuvant treatment for breast cancer.
Imm↑, Uncaria tomentosa enables the stimulation of the immune system, increasing resistance to diseases
Dose↝, Treatment using a daily dose of 300 mg dry Ut extract was effective in reducing the main chemotherapy effect, which is neutropenia.
*Inflam↓, widely used for inflammatory disorders and was previously described as an inhibitor of NF-kappaB
*NF-kB↓,
*DPPH↓, Cat's claw was an effective scavenger of DPPH
*TNF-α↓, more importantly a remarkably potent inhibitor of TNFalpha production
*Imm↑, primary mechanism for cat's claw anti-inflammatory actions appears to be immunomodulation via suppression of TNFalpha synthesis
*hepatoP↑, CA possesses a wide range of pharmacological properties, such as hepatoprotective, antimicrobial, immunomodulatory, antioxidant, antidiabetic, and anticancer activities.
*Bacteria↓,
*Imm↑,
*antiOx↑,
*AntiDiabetic↓,
*AntiCan↑,
TumCCA↑, CA can exert anticancer activity by inhibiting the cell cycle, triggering apoptosis, and suppressing the proliferation of cancer cells.
Apoptosis↑,
TumCP↓,
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NF-kB↓, reported that chlorogenic acid (CGA), a potent NF‑κB inhibitor derived from coffee, exerted antitumor activity in breast cancer.
AntiTum↑,
tumCV↓, CGA inhibited viability and proliferation in breast cancer cells.
TumCP↓,
Apoptosis↑, CGA significantly induced apoptosis and suppressed migration and invasion in breast cancer cells.
TumCMig↓,
TumCI↓,
EMT↓, CGA markedly impaired the NF‑κB and EMT signaling pathways.
TumCG↓, results revealed that CGA markedly retarded tumor growth and prolonged the survival rate of tumor‑bearing mice.
OS↑,
TumMeta↓, GA inhibited pulmonary metastasis of 4T1 cells by enhancing the proportion of CD4+ and CD8+ T cells in spleens of mice, which indicated an improvement of antitumor immunity.
CD4+↑,
CD8+↑,
Imm↑, CGA suppresses the pulmonary metastasis of breast cancer by enhancing antitumor immunity
*Imm↑, Chitosan is capable to stimulate immune responses.
*BioAv↑, By attaching galactose molecules to the chitosan molecules, a new water-soluble compound, glycated chitosan (GC), was synthesized.
eff↑, GC was designed for immune stimulations in combination with phototherapies in the treatment of metastatic tumors.
*toxicity↓, No toxic effects of GC were observed in cultured cells or in animal studies. I
*TNF-α↑, immunological effect of GC was investigated through its stimulation of TNFα secretion by macrophages in vitro.
*Obesity↓, a dietary supplement for weight loss
other↑, Nanoscale systems based on natural polymers like chitosan have garnered significant attention as promising platforms for cancer diagnosis and therapy owing to chitosan's inherent biocompatibility, biodegradability, nontoxicity, and ease of functional
Imm↑, The immunomodulatory effects of chitosan and its role in impacting the tumor microenvironment are analyzed.
DDS↑,
other↝, A common method for the synthesis of chitosan is the deacetylation of chitin using sodium hydroxide in excess as a reagent and water as a solvent
other↝, molecular weight of chitosan is between 3800 and 20,000 Daltons. The degree of deacetylation (%DD) ranges from 60% to 100%.
*Weight↝, chitosan and fat is not very well understood and has not been proved clinically yet, chitosan has been used as an effective complement to help lose weight during diet period or to stabilise one's weight
*toxicity↓, Since they are biocompatible, biodegradable, mucoadhesive, and nontoxic, with antimicrobial, antiviral, and adjuvant properties, chitin and chitosan have been widely applied in medicine and pharmacy
*Bacteria↓,
*BioAv↑,
DDS↑, Combined with drugs such as doxorubicin, paclitaxel, docetaxel, and norcantharidin, chitin and chitosan are used as drug carriers.
*Wound Healing↑, Moreover, chitin has some unusual properties that accelerate healing of wounds in humans
*other↝, Because of its mucoadhesive properties, chitin and chitosan are widely applied for mucosal routes of administration, that is, oral, nasal, and ocular mucosa, which are noninvasive routes.
*Imm↑, hypothesized that a viscous chitosan solution, when administered subcutaneously, would not only provide immune stimulation as previously
eff↑, With the development of nanotechnology, chitosan have shown its unique advantages when combined with nanoparticles.
*BioAv↝, Chitosan is soluble in diluted acids but is relatively insoluble in water [66, 67]. The poor solubility of chitosan poses limitations for its biomedical applications.
*BioAv↑, By attaching galactose molecules to the chitosan molecules, a new water-soluble compound, glycated chitosan (GC), was formed
eff↑, Chitosan nanoparticles (CNPs) can be administrated through noninvasive routes such as oral, nasal, pulmonary, and ocular routes
NK cell↑, CNP remarkably increased the killing activities of NK cells activity
IL2↑, CNP also significantly promoted the production of Th1 (IL-2 and IFN-γ) and Th2 (IL-10) cytokines
IFN-γ↑,
IL10↑,
DDS↑, various biomedical applications, including drug delivery, cartilage repair, wound healing, and tissue engineering, because of its unique physicochemical properties.
*Cartilage↑,
*Wound Healing↑,
Imm↑, investigation of the immunomodulatory properties of chitosan, since the biopolymer has been shown to modulate the maturation, activation, cytokine production, and polarization of dendritic cells and macrophages
cGAS–STING↑, Several signaling pathways, including the cGAS–STING, STAT-1, and NLRP3 inflammasomes, are involved in chitosan-induced immunomodulation. CS activates the cGAS–STING signaling pathway
STAT1↑, One crucial factor is DDA, as it was observed that 80% DDA CS activated the STAT-1 pathway, whereas 98% DDA did not
NLRP3↑, activation of the NLRP3 inflammasome by CS requires the presence of mitochondrial ROS.
*DCells↑, CS has been studied for its potential impact on DC activation, which is a crucial step in initiating the immune response.
*IL10↓, The use of CS also reduced IL-10 production and increased TGF-β1, TNF-α, and interleukin-1 beta (IL-1β) (p < 0.001) levels.
*TGF-β1↓,
*TNF-α↓,
IL1β↓,
ROS↑, CS internalization in DCs caused mitochondrial stress and led to the production of reactive oxygen species (ROS)
Wound Healing↑, possible mechanisms of how chitosan enhances coagulation and wound healing are also discussed.
Imm↑, demonstrate immune and antitumor effects are also discussed
AntiTum↑,
Imm↑, immunoadjuvant agent, so called glycated chitosan (GC), was used to enhance the immunological effects on tumor control.
TumMeta↓, The bioluminescent imaging showed that tumor metastasis was apparently suppressed by a combined treatment using HIFU and GC, but not in HIFU or GC alone.
eff↑,
angioG↓, Both chitosan and its various derivatives have been reported to selectively permeate through the cancer cell membranes and show anticancer activity through the cellular enzymatic, antiangiogenic, immunoenhancing, antioxidant defense mechanism, and ap
*Imm↑,
*antiOx↑,
selectivity↑, They get sequestered from noncancer cells and provide their enhanced bioavailability in cancer cells in a sustained release manner.
other↝, The degree of deacetylation (DDA) of chitin ranges from 60 to 100 % and molecular weight of commercially obtained chitosan ranges from 3800 to 20,000 Daltons.
toxicity↓, The degree of deacetylation (DDA) of chitin ranges from 60 to 100 % and molecular weight of commercially obtained chitosan ranges from 3800 to 20,000 Daltons.
BioAv↑,
eff↝, exert anticancer activity with minimal toxicity on noncancer cells [13] and such activity against different cancer cell lines significantly depends upon molecular weight and DDA [
Half-Life↑, Sustained Release Mechanism
MPT↑, Chitosan MDA-MB-231 Permeation enhancement, lowering of MMP9 activity
MMP9↓,
lipid-P↑, induction of lipid peroxidation, enhanced permeation and retention (EPR) effect
EPR↑,
NK cell↑, Immunoenhancement through increase in activity of NK cells, T cells, killer lymphocytes and cytokins.
Casp3↑, Cellular apoptosis, activation of caspase-3 and caspase-8,
Casp8↑,
TumCCA↑, Cytokine signaling cell cycle arrest, ROS activation
ROS↑,
DDS↑, CMCS has been prepared as a carrier of anticancer drug such as 5- fluorouracil, curcumin, and doxorubicin
VEGF↓, decrease in VEGF level and increase in TIMP1 level after 14-day treatment of mouse serum with CMCS in vivo.
TIMP1↑,
ChemoSen↑, The paclitaxel loaded modified glycol chitosan nanoparticles in the size of 400 nm has been found to show sustained release of paclitaxel to bring about the inhibition of MCF-7 tumor growth due to EPR effect in vitro
eff↑, Chitosan-curcumin nanoformulation has been found to show anticancer activity following the apoptotic pathways associated with DNA damage, cell-cycle blockage, and elevation of ROS levels in vivo
Imm↑, chitosan nanoparticle (CH-NP)-based platform for the next generation of vaccines to bypass the ex vivo manipulation and induce immune responses
DDS↑, attained promising recognition from researchers for improving the pharmacokinetics and pharmacodynamics of chemotherapeutics.
eff↓, CS-NPs for target-specific delivery of chemotherapeutics have also been considered.
*Bacteria↓, Owing to their inherent antimicrobial, antioxidant, wound healing, analgesic, anti-rheumatic, immunomodulatory, mucoadhesive, antiproliferative, and antimetastatic properties, CS and CS-NPs have been extensively investigated
*antiOx↑,
*Wound Healing↑,
*Imm↑,
TumCP↓,
TumMeta↓,
angioG↓, anticancer potential of CS and CS-NPs was attributed to their antiangiogenic, antioxidant, immunoenhancing, and apoptotic effects
Apoptosis↑,
ROS↑, apoptotic effect of CS-NPs is due to the generation of reactive oxygen species (ROS), which induce apoptosis and cause severe stress to the mitochondria and endoplasmic reticulum.
ER Stress↑,
BioAv↑, CS-NPs improve the rate and extent of absorption of chemotherapeutics from the site of administration owing to their prolonged residence time.
Half-Life↑,
eff↑, interesting approach employing high-intensity ultrasound was proposed by Choi et al35 to improve the penetration of CS-NPs into tumor tissues.
EPR↑, permeated CS-NPs were retained in tumor tissues for longer periods. This phenomenon is called “Enhanced Permeation and Retention (EPR)” effect.
ChemoSen↑, In addition to monodelivery, CS-NPs have shown tremendous potential for combined delivery of chemotherapeutics.
eff↑, CS-NPs have been conjugated with a variety of targeting ligands (eg, folic acid, hyaluronic acid, transferrin, antibodies, peptides, and aptamers) to enable selective intracellular delivery.
Showing Research Papers: 1 to 50 of 84
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 84
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
Catalase↓, 1, Ferroptosis↑, 1, GPx4↓, 2, GSH↓, 2, HO-1↓, 1, c-Iron↑, 1, lipid-P↓, 1, lipid-P↑, 2, MDA↓, 1, ROS↓, 1, ROS↑, 11, SOD↑, 1, xCT↓, 1,
Mitochondria & Bioenergetics ⓘ
MMP↓, 3, MPT↑, 1, mtDam↑, 2, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
ACSL4↑, 2, ALAT↓, 1, AMPK↑, 1, LDL↑, 1, SIRT1↓, 1, SREBP1↓, 1,
Cell Death ⓘ
Akt↓, 3, APAF1↑, 1, Apoptosis↓, 1, Apoptosis↑, 12, BAX↑, 3, Bcl-2↓, 3, Casp↑, 3, Casp3↓, 1, Casp3↑, 3, Casp8↑, 1, Casp9↑, 3, Cyt‑c↓, 1, Cyt‑c↑, 3, Fas↓, 1, Fas↑, 1, FasL↓, 1, Ferroptosis↑, 1, iNOS↓, 1, JNK↓, 3, JNK↑, 1, MAPK↓, 4,
Kinase & Signal Transduction ⓘ
HCAR2↑, 1,
Transcription & Epigenetics ⓘ
other↓, 1, other↑, 1, other↝, 6, PhotoS↑, 1, tumCV↓, 1,
Protein Folding & ER Stress ⓘ
ER Stress↑, 4, HSP27↓, 1,
Autophagy & Lysosomes ⓘ
ATG5↑, 1, Beclin-1↑, 2, LC3I↑, 1, TumAuto↑, 2, mt-TumAuto↑, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 2, P53↑, 2, cl‑PARP↑, 1, γH2AX↑, 1,
Cell Cycle & Senescence ⓘ
CDK4↓, 1, cycD1/CCND1↓, 3, P21↑, 2, TumCCA↑, 7,
Proliferation, Differentiation & Cell State ⓘ
CD133↓, 1, CD44↓, 2, CSCs↓, 1, EMT↓, 5, ERK↓, 4, GSK‐3β↓, 2, HDAC↓, 1, mTOR↓, 2, NOTCH↓, 1, NOTCH1↓, 3, NOTCH3↓, 1, PI3K↓, 5, STAT1↑, 1, STAT3↓, 1, TumCG↓, 7, Wnt↓, 4,
Migration ⓘ
Ca+2↑, 1, CEA↓, 1, miR-133a-3p↑, 1, MMP1↓, 1, MMP2↓, 3, MMP9↓, 5, MMPs↓, 2, TGF-β1↓, 1, TIMP1↑, 1, TumCI↓, 2, TumCMig↓, 2, TumCP↓, 7, TumMeta↓, 6, Vim↓, 2, β-catenin/ZEB1↓, 5,
Angiogenesis & Vasculature ⓘ
angioG↓, 6, EGFR↓, 1, EPR↑, 2, VEGF↓, 6, VEGFR2↓, 1,
Barriers & Transport ⓘ
P-gp↓, 2,
Immune & Inflammatory Signaling ⓘ
CD4+↑, 1, COX2↓, 2, CXCR4↓, 2, Dectin1↝, 1, HCAR2↑, 1, IFN-γ↓, 1, IFN-γ↑, 2, IL10↑, 1, IL12↑, 1, IL1β↓, 1, IL2↓, 1, IL2↑, 2, IL4↓, 1, IL6↓, 4, Imm↑, 33, Inflam↓, 2, Neut↓, 1, NF-kB↓, 6, NK cell↑, 3, PD-L1↓, 3, TNF-α↓, 2, TNF-α↑, 1,
Cellular Microenvironment ⓘ
cGAS–STING↑, 1,
Protein Aggregation ⓘ
NLRP3↓, 1, NLRP3↑, 1,
Hormonal & Nuclear Receptors ⓘ
AR↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↑, 3, BioAv↝, 1, ChemoSen↑, 14, DDS↑, 5, Dose↝, 6, eff↓, 1, eff↑, 25, eff↝, 1, Half-Life↑, 2, MDR1↓, 1, RadioS↑, 3, selectivity↑, 3,
Clinical Biomarkers ⓘ
ALAT↓, 1, AR↓, 1, CEA↓, 1, EGFR↓, 1, GutMicro↑, 5, IL6↓, 4, PD-L1↓, 3,
Functional Outcomes ⓘ
AntiCan↑, 3, AntiTum↑, 8, chemoP↑, 6, chemoPv↑, 1, OS↑, 7, QoL↑, 4, radioP↑, 2, Risk↓, 3, toxicity↓, 2, Wound Healing↑, 1,
Infection & Microbiome ⓘ
CD8+↑, 1, Dectin1↝, 1,
Total Targets: 160
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 8, Catalase↑, 3, DPPH↓, 1, GPx↑, 2, GSH↑, 2, GSTA1↑, 1, HO-1↑, 1, lipid-P↓, 1, MDA↓, 3, NRF2↑, 1, ROS↓, 4, ROS↝, 1, SOD↑, 4, TAC↑, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 2, LDH↓, 1, LDH↑, 1, LDL↓, 1,
Cell Death ⓘ
necrosis↓, 1,
Transcription & Epigenetics ⓘ
other↓, 1, other↝, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 2,
Proliferation, Differentiation & Cell State ⓘ
TRPM7↓, 1,
Migration ⓘ
5LO↓, 3, AntiAg↑, 2, Cartilage↑, 1, TGF-β1↓, 1, Treg lymp↑, 1, ZO-1↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 3, CRP↓, 1, DCells↑, 1, Dectin1↑, 1, IL10?, 1, IL10↓, 1, IL10↑, 2, IL17↓, 1, IL1β↓, 1, IL6↓, 3, IL6↑, 1, Imm↑, 18, Inflam↓, 11, NF-kB↓, 7, TNF-α↓, 7, TNF-α↑, 1,
Protein Aggregation ⓘ
NLRP3↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↑, 4, BioAv↝, 1, Dose↝, 2, eff↓, 1, eff↑, 5, eff↝, 1,
Clinical Biomarkers ⓘ
ALAT↓, 2, AST↓, 3, BP↓, 1, CRP↓, 1, GutMicro↑, 3, IL6↓, 3, IL6↑, 1, LDH↓, 1, LDH↑, 1,
Functional Outcomes ⓘ
AntiCan↑, 4, AntiDiabetic↓, 1, AntiDiabetic↑, 4, cardioP↑, 3, chemoPv↑, 1, cognitive↑, 1, hepatoP↑, 4, motorD↑, 1, neuroP↑, 3, Obesity↓, 2, Pain↓, 2, Risk↓, 1, toxicity↓, 6, toxicity↑, 1, Weight↓, 1, Weight↝, 1, Wound Healing↑, 6,
Infection & Microbiome ⓘ
Bacteria↓, 8, Dectin1↑, 1, Diar↓, 1,
Total Targets: 82
Scientific Paper Hit Count for: Imm, immunostimulatory
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#:1332 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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