Sepsis Cancer Research Results

Sepsis, Sepsis: Click to Expand ⟱
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Sepsis is a life-threatening medical condition that occurs when the body’s response to an infection causes widespread inflammation. This uncontrolled inflammatory response can lead to tissue damage, organ failure, and, in severe cases, death.

-Treatment options PKM2, Glycolysis and HIF1α inhibitors.

-Chemotherapy, radiation therapy, and immunosuppressive drugs can further weaken the immune system, making patients more susceptible to infections that can lead to sepsis.

-AgNPs have demonstrated antimicrobial effects against a wide range of pathogens including bacteria, fungi, and viruses. Since infections are the primary trigger for sepsis, their ability to reduce microbial loads has been of significant interest.
Scientific Papers found: Click to Expand⟱
3456- ALA,    Renal-Protective Roles of Lipoic Acid in Kidney Disease
- Review, NA, NA
*RenoP↑, We focus on various animal models of kidney injury by which the underlying renoprotective mechanisms of ALA have been unraveled
*ROS↓, ALA’s renal protective actions that include decreasing oxidative damage, increasing antioxidant capacities, counteracting inflammation, mitigating renal fibrosis, and attenuating nephron cell death.
*antiOx↑,
*Inflam↓,
*Sepsis↓, figure 1
*IronCh↑, ALA can also chelate metals such as zinc, iron, and copper and regenerate endogenous antioxidants—such as glutathione—and exogenous vitamin antioxidants—such as vitamins C and E—with minimal side effects
*BUN↓, ALA can decrease acute kidney injury by lowering serum blood urea nitrogen, creatinine levels, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β), thereby decreasing endothelin-1 vasoconstriction, neutrophil dif
*creat↓,
*TNF-α↓,
*IL6↓,
*IL1β↓,
*MDA↓, pretreatment with ALA decreased MDA content and ameliorated renal oxidative stress
*NRF2↑, activate the Nrf2 signaling pathway, leading to upregulation of the second-phase cytoprotective proteins such as heme oxygenase-1 (HO-1) and NAD(P)H quinone dehydrogenase 1 (NQO1)
*HO-1↑,
*NQO1↑,
*chemoP↑, ALA has also been shown to lower plasma creatinine levels and urine output, increase creatinine clearance and urine osmolality, and normalize sodium excretion in cisplatin kidney injury
*eff↑, ALA can also minimize renal toxicity induced by gold nanoparticles, which are often used as drug carriers
*NF-kB↓, Enhancing autophagy, inhibiting NF-KB, attenuating mitochondrial oxidative stress

2292- Ba,  BA,    Baicalin and baicalein in modulating tumor microenvironment for cancer treatment: A comprehensive review with future perspectives
- Review, Var, NA
AntiCan↑, Baicalin and baicalein exhibit anticancer activities against multiple cancers with extremely low toxicity to normal cells.
*toxicity↓,
BioAv↝, Baicalein permeates easily through the epithelium from the gut lumen to the blood underneath due to its low molecular mass and high lipophilicity, albeit a low presence of its transporters.
BioAv↓, In contrast, baicalin has limited permeability partly due to its larger molecular mass and higher hydrophilicity [24]. The overall low water solubility of baicalin and baicalein contributes to their poor bioavailability.
*ROS↓, baicalin protected macrophages against mycoplasma gallisepticum (MG)-induced ROS production and NLRP3 inflammasome activation by upregulating autophagy and TLR2-NFκB pathway
*TLR2↓,
*NF-kB↓,
*NRF2↑, Therefore, baicalin exerts strong antioxidant activity by activating NRF2 antioxidant program.
*antiOx↑,
*Inflam↓, These data suggest that by attenuating ROS and inflammation baicalein inhibits tumor formation and metastasis.
HDAC1↓, baicalein reduced CTCLs by inhibiting HDAC1 and HDAC8 and its effect on tumor inhibition was better than traditional HDAC inhibitors
HDAC8↓,
Wnt↓, Baicalein also reduced the proliferation of acute T-lymphoblastic leukemia (TLL) Jurkat cells by inhibiting the Wnt/β-catenin signaling pathway
β-catenin/ZEB1↓,
PD-L1↓, baicalein and baicalin promoted antitumor immune response by suppressing PD-L1 expression of HCC cells, thus increasing tumor regression
Sepsis↓, Baicalein can also attenuate severe sepsis via ameliorating immune dysfunction of T lymphocytes.
NF-kB↓, downregulation of NFκB and CD74/CD44 signaling in EBV-transformed B cells
LOX1↓, baicalein is considered to be an inhibitor of lipoxygenases (LOXs)
COX2↓, inhibits the expression of NF-κB/p65 and COX-2
VEGF↑, Baicalin was shown to suppress the expression of VEGF, resulting in the inhibition of PI3K/AKT/mTOR pathway and reduction of proliferation and migration of human mesothelioma cells
PI3K↓,
Akt↓,
mTOR↓,
MMP2↓, baicalin suppressed expression of MMP-2 and MMP-9 via restriction of p38MAPK signaling, resulting in reduced breast cancer cell growth, invasion
MMP9↓,
SIRT1↑, The inhibition of MMP-2 and MMP-9 expression in NSCLC cells is mediated by activating the SIRT1/AMPK signaling pathway.
AMPK↑,

2760- BetA,    A Review on Preparation of Betulinic Acid and Its Biological Activities
- Review, Var, NA - Review, Stroke, NA
AntiTum↑, BA is considered a future promising antitumor compound
Cyt‑c↑, BA stimulated mitochondria to release cytochrome c and Smac and cause further apoptosis reactions
Smad1↑,
Sepsis↓, Administration of 10 and 30 mg/kg of BA significantly improved survival against sepsis and attenuated lung injury.
NF-kB↓, BA inhibited nuclear factor-kappa B (NF-κB) expression in the lung and decreased levels of cytokine, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1) and matrix metalloproteinase-9 (MMP-9)
ICAM-1↓,
MCP1↓,
MMP9↓,
COX2↓, In hPBMCs, BA suppressed cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PEG2) production by inhibiting extracellular regulated kinase (ERK) and Akt phosphorylation and thereby modulated the NF-κB signaling pathway
PGE2↓,
ERK↓,
p‑Akt↓,
*ROS↓, BA significantly decreased the mortality of mice against endotoxin shock and inhibited the production of PEG2 in two of the most susceptible organs, lungs and livers [80]. Moreover, BA reduced reactive oxygen species (ROS) formation
*LDH↓, and the release of lactate dehydrogenase
*hepatoP↑, hepatoprotective effect of BA from Tecomella undulata.
*SOD↑, Pretreatment of BA prevented the depletion of hepatic antioxidants superoxide dismutase (SOD) and catalase (CAT), reduced glutathione (GSH) and ascorbic acid (AA) and decreased the CCl4-induced LPO level
*Catalase↑,
*GSH↑,
*AST↓, A also attenuated the elevation of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) plasma level,
*ALAT↓,
*RenoP↑, BA also exhibits renal-protective effects. Renal fibrosis is an end-stage renal disease symptom that develops from chronic kidney disease (CKD).
*ROS↓, BA protected against this ischemia-reperfusion injury in a mice model by enhancing blood flow and reducing oxidative stress and nitrosative stress
*α-SMA↓, Moreover, BA reduced the expression of α-smooth muscle actin (α-SMA) and collagen-I

2347- CAP,    Capsaicin ameliorates inflammation in a TRPV1-independent mechanism by inhibiting PKM2-LDHA-mediated Warburg effect in sepsis
- in-vivo, Nor, NA - in-vitro, Nor, RAW264.7
*PKM2↓, capsaicin directly binds to and inhibits PKM2 and LDHA, and further suppresses the Warburg effect in inflammatory macrophages.
*LDHA↓,
*Warburg↓,
*COX2↓, capsaicin targets COX-2 and downregulates its expression in vivo and in vitro.
*Sepsis↓, may function as a novel agent for sepsis and inflammation treatment.
*Inflam↓,
*ECAR↓, CAP notably reduced the ECAR
*OCR↑, LPS decreased the OCR by inhibiting the mitochondrial respiration, and CAP could reverse this decrease

2348- CAP,    Recent advances in analysis of capsaicin and its effects on metabolic pathways by mass spectrometry
- Analysis, Nor, NA
Warburg↓, Capsaicin inhibits the Warburg effect by binding directly to Cys424 residue and LDHA of pyruvate kinase isoenzyme type M2 (PKM2).
*PKM2↓,
*COX2↓, capsaicin targets COX-2 and down-regulates its expression, which results in the further inhibition of inflammation
*Inflam↓,
*Sepsis↓, capsaicin may be used as a new active ingredient to treat sepsis and inflammation
*AMPK↑, capsaicin activates adenylate-activated protein kinase (AMPK) and protein kinase A (PKA), in turn enhancing the activity of the mitochondrial respiratory chain and promoting fatty acid oxidation
*PKA↑,
*mitResp↑,
*FAO↑,
*FASN↓, capsaicin can inhibit the activity of fatty acid synthetase
*PGM1?,
*ATP↑, treatment resulted in increased intracellular ATP levels (the end product of glycolysis)
*ROS↓, Capsaicin can mitigate the negative effects of oxidative stress on human health by scavenging these free radicals and reducing the oxidative stress response.

3869- Carno,    Carnosine, Small but Mighty—Prospect of Use as Functional Ingredient for Functional Food Formulation
- Review, AD, NA - Review, Stroke, NA
*ROS↓, carnosine scavenges reactive oxygen species (ROS)
*IronCh↑, it can chelate divalent metal ions: heavy metal chelating activity
*AntiAge↑, can slow down aging.
*antiOx↑, natural antioxidant [4] and has anti-inflammatory and neuroprotective properties
*Inflam↓,
*neuroP↑,
*lipid-P↓, Carnosine reduces lipid peroxidation, but also inhibits oxidative modification of protein exposed to hydroxyl radicals
*toxicity↓, carnosine can be recommended as a natural cure that has no side effects but is highly efficient
*NOX4↓, human kidney tubular epithelial (HK2) cells indicated that carnosine decreased NADPH oxidase (Nox) 4 expression and increased total superoxide dismutase (T-SOD) activity, thus reducing the production of intracellular ROS,
*SOD↑,
*HNE↓, Rising data indicate that carnosine acts as a scavenger of reactive and cytotoxic carbonyl species including 4-hydroxynonenal (HNE)
*IL6↓, anserine and/or carnosine supplementation significantly decreased IL-6, TNF-α, and IL-1β in pre-treated mice with MPTP-induced PD,
*TNF-α↓,
*IL1β↓,
*Sepsis↓, carnosine has a beneficial effect on reducing acute kidney injury due to septic shock
*eff↑, carnosine on ischemic stroke, there was a 29.4% average reduction in infarct volume with a clear dose-dependent effect (38.1% reduction on 1000 mg/kg dose compared with 13.2% for doses less than 500 mg/kg)
*GABA↝, In addition to the carnosine-histidine-histamine pathway, carnosine can also have a direct impact on CA1 pyramidal neurons [212] or act as a precursor for the neurotransmitter GABA
*Aβ↓, Several studies have reported that carnosine supplementation reduced β-amyloid cumulation in the hippocampus of a transgenic mouse model of AD
Glycolysis↓, carnosine has the ability to inhibit glycolysis and thus achieve an antitumor effect
AntiTum↑,
p‑Akt↓, significant reduction of Akt phosphorylation in the U87 glioblastoma cell line
TumCCA↑, Carnosine has an effect in bladder cancer by stopping the G1 phase cell cycle by increasing p21WAF1 expression and decreasing cyclin/CDK complexes
angioG↓, inhibits angiogenesis by suppressing VEGFR-2
VEGFR2↓,
NF-kB↓, suppressing nuclear factor kB (NF-κB) signaling pathway activation in human colon cancer cells

4914- DSF,  immuno,    Disulfiram and cancer immunotherapy: Advanced nano-delivery systems and potential therapeutic strategies
- Review, Var, NA
AntiTum↑, potential as an anti-tumor agent and even as an enhancer of cancer immunotherapy
eff↑, Targeted delivery: through nanotechnology, specific delivery of disulfiram to tumor sites can be achieved to minimize damage to normal tissues and increase drug accumulation in tumor cells
ALDH↓, It works by inhibiting an enzyme called Aldehyde Dehydrogenase (ALDH).
Dose↝, DSF is not only affordable at $20–40 for a daily dose of 250 mg taken orally in the USA, but it is also considered to be safe, allowing for long-term treatment at the same dosage.
RadioS↑, DSF/Cu can enhance the effects of ionizing radiation and induce ICD in breast cancer
angioG↓, inhibition of angiogenesis and metastasis, make it a versatile agent in combating cancer
TumMeta↓,
BioAv↝, limitations associated with its delivery, solubility, and off-target toxicity have prompted the development of innovative strategies to improve its clinical efficacy
ROS↑, DSF effectively treats tumors. Such as increasing the production of ROS, causing DNA damage, and impeding enzyme activity.
DNAdam↑,
P-gp↓, DSF can target P-glycoprotein (P-gp) dysfunction, cancer stem cells (CSCs), and hinder the process of epithelial-mesenchymal transition (EMT).
CSCs↓,
EMT↓,
Imm↑, DSF stimulates the immune system
SOD↓, generation of ROS, inhibition of the superoxide dismutase activity and activation of the mitogen-activated protein kinase (MAPK)
MAPK↓,
NF-kB↓, NF-κB inhibiting activity of DSF could be attributed to their inhibition of the proteasome and degradation other regulatory redox-sensitive proteins.
ChemoSen↑, therapeutic effect of combining DSF with conventional cancer drugs like cisplatin and doxorubicin (DOX) has been proven to be enhanced.
eff↑, combination use of DSF with immunotherapy has shown remarkable success in preclinical and clinical studies.
toxicity↝, The administration of disulfiram necessitates the complete abstinence from alcohol
BioAv↑, researchers use lipid nanoparticles as carriers for disulfiram and used to improve its bioavailability and reduce side effects.
*Inflam↓, DSF has the ability to inhibit inflammation, which has potential applications in treating various inflammatory diseases,
Sepsis↓, Mice with sepsis experienced reduced mortality when administered with DSF-loaded lactoferrin nanoparticles,

2515- H2,    Recent Advances in Studies of Molecular Hydrogen against Sepsis
- Review, Sepsis, NA
*Sepsis↓, Molecular hydrogen exerts multiple biological effects involving anti-inflammation, anti-oxidation, anti-apoptosis, anti-shock, and autophagy regulation, which may attenuate the organ and barrier damage caused by sepsis.
*Inflam↓,
*antiOx↑,
*ROS↓, Studies have demonstrated that HRS reduces ROS production and attenuates mitochondrial dysfunction by inhibiting NADPH oxidase activity in rat cardiomyocytes
*NADPH↓,

2508- H2,    Molecular hydrogen is a promising therapeutic agent for pulmonary disease
- Review, Var, NA - Review, Sepsis, NA
*ROS↓, inhalation of 2% molecular hydrogen results in the selective scavenging of hydroxyl free radical (·OH) and peroxynitrite anion (ONOO-), significantly improving oxidative stress injury caused by cerebral ischemia/reperfusion (I/R)
eff↝, Molecular hydrogen can exert biological effects on almost all organs, including the brain, heart, lung, liver, and pancreas.
*Inflam↓, including roles in the regulation of oxidative stress and anti-inflammatory and anti-apoptotic effects
*NRF2↑, By stimulating nuclear factor erythroid 2-related factor 2 (Nrf2), which regulates the basal and induces expression of many antioxidant enzymes
*HO-1↑, hydrogen can increase the expression of heme oxygenase-1 (HO-1)
*SOD↑, increases the activity of the antioxidant enzymes SOD, CAT, and myeloperoxidase (MPO)
*Catalase↑,
*MPO↑,
*ASK1↓, Molecular hydrogen can block the apoptosis signal-regulating kinase 1 (ASK1) signaling pathway
*NADPH↓, thereby inhibiting nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and decreasing free radical production
*Sepsis↓, Emerging evidence suggests that hydrogen can prevent sepsis, providing a novel treatment strategy for sepsis-induced ALI.
*HMGB1↓, Hydrogen attenuates tissue injury and dysfunction by inhibiting HMGB-1.
ROS↑, it has been shown that hydrogen pretreatment enhances ROS and the expression of pyroptosis-related proteins, stimulates NLRP3 inflammasome/gasdermin D (GSDMD) activation, and inhibits endometrial cancer
NLRP3↑,
GSDMD↑,
chemoP↑, Hydrogen can alleviate the side effects of conventional anti-cancer therapies, such as chemotherapy and radiotherapy, and improve quality of life
eff↑, It significantly improves the physical status of patients, reduces fatigue, insomnia, anorexia, and pain, and decreases elevated tumor markers.

3770- H2,    Role of Molecular Hydrogen in Ageing and Ageing-Related Diseases
- Review, AD, NA - Review, Park, NA
*antiOx↑, antioxidative properties as it directly neutralizes hydroxyl radicals and reduces peroxynitrite level
*NRF2↑, activates Nrf2 and HO-1, which regulate many antioxidant enzymes and proteasomes.
*HO-1↑,
*Inflam↓, hydrogen may prevent inflammation
*neuroP↑, prevention and treatment of various ageing-related diseases, such as neurodegenerative disorders, cardiovascular disease, pulmonary disease, diabetes, and cancer.
*cardioP↑,
*other↓, It also prevented ischemia-reperfusion (I/R) injury and stroke in a rat model
*ROS↓, H2 has been shown to exert its beneficial effects in various pathological conditions that involve free radicals and oxidative stress
*NADPH↓, figure 2, H2 Inhibits NADPH Oxidase Activity
*Catalase↑,
*GPx1↑,
*NO↓, H2 Indirectly Reduces Nitric Oxide (NO) Production
*mt-ROS↓, H2 Decreases Mitochondrial ROS
*SIRT3↑, In the kidneys, H2 suppressed the downregulated Sirt3 expression, which is the most abundant member of the sirtuin family, by reducing oxidative stress reactions
*SIRT1↑, In the liver, H2 elevated HO-1 to induce Sirt1 expression
*TLR4↓, H2 inhibits TLR4, which involves hyperglycemia in type 2 diabetes mellitus
*mTOR↓, For example, H2 inhibits mTOR, activates autophagy, and alleviates cognitive impairment resulting from sepsis
*cognitive↑,
*Sepsis↓,
*PTEN↓, It inhibits the activation of the PTEN/AKT/mTOR pathway and alleviates peritoneal fibrosis
*Akt↓,
*NLRP3↓, It also facilitates autophagy-mediated NLRP3 inflammasome inactivation and alleviates mitochondrial dysfunction and organ damage
*AntiAg↑, antiageing mechanism of H2 and the influence on ageing hallmarks are summarized in Figure 3.
*IL6↓, significantly suppressed inflammatory cytokines (IL-6, TNF-α, and IL-1β), MDA, and 8-OHdG, and improved memory dysfunction
*TNF-α↓,
*IL1β↓,
*MDA↓,
*memory↑,
*FOXO3↑, HRW can also upregulate Sirt1-Forkhead box protein O3a (FOXO3a
TumCG↓, H2 inhibits lung cancer progression
*LDL↓, Decreases oxidized LDL; improves HDL function

3773- H2,    Role and mechanism of molecular hydrogen in the treatment of Parkinson’s diseases
- Review, Park, NA
*neuroP↑, potential neuroprotective effects, attributed to its selective antioxidant and anti-inflammatory properties.
*antiOx↑,
*Inflam↓,
*ROS↓, potential of molecular hydrogen to attenuate oxidative stress,
*NADPH↓, via the inhibition of NADPH oxidase activity
*NRF2↑, it also enhances the endogenous defense system by modulating the Nrf2/ARE pathway.
*BBB↑, easily penetrate the blood–brain barrier
*IL1β↓, H₂ significantly reduces the release of pro-inflammatory factors, including IL-1β, IL-6, TNF-α, NF-κB, and HMGB1,
*IL6↓,
*TNF-α↓,
*NF-kB↓,
*NLRP3↓, hydrogen can mitigate neuroinflammation by inhibiting the NLRP3 inflammasome pathway
*Sepsis↓, hydrogen intervention in sepsis models
*p‑mTOR↓, inhibits the phosphorylation level of mTOR (indicated by a decrease in the p-mTOR/mTOR ratio) while activating the AMPK s
*AMPK↑,
*SIRT1↑, hydrogen-rich water alleviates intestinal oxidative stress by upregulating the expression of SIRT1, Nrf2, and HO-1
*HO-1↑,

3787- H2,    Hydrogen, a Novel Therapeutic Molecule, Regulates Oxidative Stress, Inflammation, and Apoptosis
- Review, AD, NA
*Inflam↓, anti-inflammatory and antioxidant activity
*antiOx↑,
*ROS↓, annihilating excess reactive oxygen species production and modulating nuclear transcription factor.
*other↝, H2 does not explode if it is <10% when mixed with air or O2
*NF-kB↓, H2-rich saline inhibited the activation of crucial inflammatory signaling pathway NF-κB and reduced serum IL-1β, IL-6, and TNF-α levels,
*IL2↓,
*IL6↓,
*TNF-α↓,
*HO-1↑, Studies have demonstrated that H2 administration increased the HO-1 expression
Apoptosis↑, Similarly, cell apoptosis and autophagy were significantly enhanced in A549 and H1975 lung cancer cell lines treated with different concentrations of H2 gas
TumAuto↑,
*Sepsis↓, sepsis-related organ injury models, H2 treatment significantly reduced the expression of caspase-1 in the damaged organ and the levels of IL-1β and IL-18 cytokines
*NLRP3↓, NLRP3, caspase-1, and the N-terminal of gasdermin D (GSDMD-N), were reduced after lung inflation with 3% H2,
Pyro↑, H2-rich water inhibited the proliferation of endometrial cancer cells by triggering the NLRP3 inflammasome/caspase-1 mediated classical pyroptosis pathway and activated the downstream proinflammatory cytokine IL-1β.

3257- PBG,    The Potential Use of Propolis as a Primary or an Adjunctive Therapy in Respiratory Tract-Related Diseases and Disorders: A Systematic Scoping Review
- Review, Var, NA
CDK4↓, CAPE also induces G1 phase cell arrest by lowering the expression of CDK4, CDK6, Rb, and p-Rb. M
CDK6↓,
pRB↓,
ROS↓, Artepillin C, a bioactive component of Brazilian green propolis, reduces oxidative damage markers, namely 4-HNE-modified proteins, 8-OHdG, malonaldehyde, and thiobarbituric acid reactive substances in lung tissues with pulmonary adenocarcinoma
TumCCA↑, Propolin, a novel component of prenylflavanones in Taiwanese propolis, was demonstrated to have anti-cancer properties. Propolin H induces cell arrest at G1 phase and upregulates the expression of p21
P21↑,
PI3K↓, Propolin C also inhibits PI3K/Akt and ERK-mediated epithelial-to-mesenchymal transition by upregulating E-cadherin (epithelial cell marker) and downregulating vimentin
Akt↓,
EMT↓,
E-cadherin↑,
Vim↓,
*COX2↓, bioactive compounds such as CAPE, galangin significantly reduce the activity of lung cyclooxygenase (COX) and myeloperoxidase (MPO), and malonaldehyde (MDA), TNF-α, and IL-6 levels, while increasing the activity of catalase (CAT) and SOD
*MPO↓,
*MDA↓,
*TNF-α↓,
*IL6↓,
*Catalase↑,
*SOD↑,
*AST↓, Chrysin also reduces the expression of oxidative and inflammatory markers such as aspartate transaminase (AST), alanine aminotransferase (ALT), IL-1β, IL-10, TNF-α, and MDA levels and increases the antioxidant parameters such as SOD, CAT, and GPx
*ALAT↓,
*IL1β↓,
*IL10↓,
*GPx↓,
*TLR4↓, propolis also inhibits the expression of Toll-like receptor 4 (TLR4), macrophage infiltration, MPO activity, and apoptosis of lung tissues in septic animals
*Sepsis↓,
*IFN-γ↑, CAPE also significantly increases IFN-γ
*GSH↑, propolis significantly increased the level of GSH and the histological appearances of propolis-treated bleomycin-induced pulmonary fibrosis rats.
*NRF2↑, CAPE significantly increases the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2)
*α-SMA↓, propolis significantly inhibits the expression of α- SMA, collagen fibers, and TGF-1β.
*TGF-β↓,
*IL5↓, Propolis also inhibits the expression of inflammatory cytokines and chemokines such as TNF-α, IL-5, IL-6, IL-8, IL-10, NF-kB, IFN-γ, PGF2a, and PGE2.
*IL6↓,
*IL8↓,
*PGE2↓,
*NF-kB↓,
*MMP9↓, downregulating the expression of TGF-1β, ICAM-1, α-SMA, MMP-9, IgE, and IgG1.

4965- PSO,  Cisplatin,    The synergistic antitumor effects of psoralidin and cisplatin in gastric cancer by inducing ACSL4-mediated ferroptosis
- vitro+vivo, GC, HGC27 - vitro+vivo, GC, MKN45
TumCP↓, PSO impeded GC cell proliferation, migration, invasion, and growth in vivo.
TumCMig↓,
TumCI↓,
TumCG↓,
*toxicity↓, PSO exhibited no significant toxic effects on organs and mitigated DDP-mediated liver and kidney injuries.
eff↑, The combination of PSO and DDP exhibited enhanced inhibitory functions
Ferroptosis↑, PSO and DDP can significantly promote GC cell ferroptosis.
ACSL4↑, PSO promoted ACSL4 expression and suppressed GPX4, AIFM2, and SLC7A11.
GPx4↓,
ChemoSen↑, PSO may serve as a nontoxic adjuvant to enhance DDP’s efficacy and reduce side effects in GC.
chemoP↑,
AntiTum↑, Moreover, we found that the combination of PSO and DDP had synergistic antitumor effects on GC.
Sepsis↓, PSO has protective effects against sepsis-induced acute lung injury [40] and myocardial injury [41] at a dose of 50 mg/kg.

2339- QC,    Quercetin protects against LPS-induced lung injury in mice via SIRT1-mediated suppression of PKM2 nuclear accumulation
- in-vivo, Nor, NA
*Inflam↓, Quercetin (Que) is a natural bioflavonoid compound with anti-inflammatory and antioxidative properties that reportedly inhibits the NLRP3 inflammasome in sepsis-induced organ dysfunctions such as ALI
*antiOx↑,
*NLRP3↓,
*Sepsis↓,
*PKM2↓, inhibit the activation of the NLRP3 inflammasome by suppressing the nuclear accumulation of PKM2 and increasing SIRT1 levels.
*SIRT1↓,

3349- QC,    Sepsis_via_Inhibition_of_Reactive_Oxygen_Species_ROS_and_Downregulation_of_High_Mobility_Group_Box_1_HMGB1_Protein_Expression">Quercetin Exerted Protective Effects in a Rat Model of Sepsis via Inhibition of Reactive Oxygen Species (ROS) and Downregulation of High Mobility Group Box 1 (HMGB1) Protein Expression
- in-vivo, Sepsis, NA
*Sepsis↓, results showed that quercetin reduced the tissue edema, congestion, and hemorrhage, increased the alveolar volume, and helped to maintain the lung anatomy of septic rats.
*ROS↓, Admistration of quercetin at the dosage of 15 and 20 mg/kg to septic rats caused significant reduction in the ROS levels.
*SOD↑, The results showed that administration of quercetin at the dosage of 15 and 5 mg/kg to septic rats caused a significant increase in SOD, CAT, and APX expression levels
*Catalase↑,
*HMGB1↓, quercetin caused a significant decrease in HMGB1 protein levels
*Inflam↓, quercetin was found to reduce the inflammation associated with sepsis
*TAC↑, significant increase in the expression of antioxidant enzymes.

3365- QC,    Quercetin attenuates sepsis-induced acute lung injury via suppressing oxidative stress-mediated ER stress through activation of SIRT1/AMPK pathways
- in-vivo, Sepsis, NA
*ER Stress↓, quercetin could inhibit the level of ER stress as evidenced by decreased mRNA expression of PDI, CHOP, GRP78, ATF6, PERK, IRE1α
*PDI↓,
*CHOP↓,
*GRP78/BiP↓,
*ATF6↓,
*PERK↓,
*IRE1↓,
*MMP↑, and improve mitochondrial function, as presented by increased MMP, SOD level and reduced production of ROS, MDA.
*SOD↑,
*ROS↓,
*MDA↓,
*SIRT1↑, quercetin upregulated SIRT1/AMPK mRNA expression.
*AMPK↑,
*Sepsis↓, quercetin could protect against sepsis-induced ALI by suppressing oxidative stress-mediated ER stress and mitochondrial dysfunction via induction of the SIRT1/AMPK pathways.

3021- RosA,    Rosmarinic acid ameliorates septic-associated mortality and lung injury in mice via GRP78/IRE1α/JNK pathway
- in-vivo, Sepsis, NA
*eff↑, RA (40 mg/kg) significantly decreased mortality and alleviated septic-associated lung injury.
*SOD↑, RA significantly reversed LPS induced decrease in serum T-aoc level and superoxide dismutase (SOD) activity, and increase in malondialdehyde (MDA) activity.
*MDA↓,
*GRP78/BiP↓, LPS induced activation of GRP78/IRE1α/JNK pathway was suppressed by RA pretreatment.
*IRE1↓,
*JNK↓,
*Sepsis↓,

3023- RosA,    Rosmarinic acid alleviates septic acute respiratory distress syndrome in mice by suppressing the bronchial epithelial RAS-mediated ferroptosis
- in-vivo, Sepsis, NA
*GPx4↑, RA notably inhibited the infiltration into the lungs of neutrophils and monocytes with increased amounts of GPX4 and ACE2 proteins, lung function improvement,
*Inflam↓, decreased inflammatory cytokines levels and ER stress in LPS-induced ARDS in mice.
*ER Stress↓,
*Ferroptosis↓, the anti-ferroptosis effect of RA in LPS-induced septic
*Sepsis↓,
*GRP78/BiP↓, Previously, we reported that RA markedly ameliorated septic-associated mortality and lung injury via inhibiting GRP78/IRE1α/JNK pathway-mediated ERS
*IRE1↓,
JNK↓,

3024- RosA,    rmMANF prevents sepsis-associated lung injury via inhibiting endoplasmic reticulum stress-induced ferroptosis in mice
- in-vivo, Sepsis, NA
*Ferroptosis↓, rmMANF pretreatment inhibits ferroptosis by suppressing GRP78/PERK/ATF4 axis.
*GRP78/BiP↓,
*PERK↓,
*ATF4↓,
*Sepsis↓,
*GSH↑, LPS administration mice exhibited elevated MDA immunoactivity, total iron level, and declined GSH level, and SOD, CAT activities, while these effects of LPS were effectively against by rmMANF pretreatment
*SOD↑,
*Catalase↑,

4607- SeNPs,  AgNPs,    A Review on synthesis and their antibacterial activity of Silver and Selenium nanoparticles against biofilm forming Staphylococcus aureus
- Review, NA, NA
*Bacteria↓, antibacterial activity of Silver and Selenium nanoparticles against biofilm forming Staphylococcus aureus
*eff↑, Ag-based antiseptics that may be linked to broad-spectrum activity and far lower propensity to induce microbial resistance than antibiotics
ROS↑, In general, certain selenium compounds are catalytic and produce ROS by their interactionwith thiols, such as reduced glutathione, forming the glutathione selenide anion, GSSe. ̄ ... produced ROS which kills tumor cells
*Dose↝, According to the World Health Organization (WHO), a recommendeddaily dietary selenium intake is 40 μg Se/day
*eff↑, Silver coating of medical devices is believed to preserve infection resistance
toxicity↝, Exact mechanism of selenium toxicity remains unclear but there are many data about its prooxidant effect particularly in the form of selenite,while selenomethionine and selenocysteine are less toxic.
*Sepsis↓, We postulated that high-conc. supplementation of sodium-selenite would recover the outcome of patients with severe sepsis.(14 daily constant infusions of 1000 μg intravenously)
*other↝, Selenium is an essential dietary nutrient for most animals and humans, which is incorporated into twelve or more known proteins or enzymes as an amino acid, selenocysteine.
eff↑, Selenodiglutathione is the most potent selenium compound against cancer cells and readily arrests their growth as compared to selenite and any other selenium compound.

2354- SK,    PKM2-dependent glycolysis promotes NLRP3 and AIM2 inflammasome activation
- in-vivo, Sepsis, NA
PKM2↓, Shikonin is a potent PKM2 inhibitor in cancer cells and macrophages
*PKM2↓,
*IL1β↓, Shikonin dose-dependently inhibited IL-1β, IL-18 and HMGB1 release in activated BMDMs following treatment with NLRP3 inflammasome activator (for example, ATP) or AIM2 inflammasome activator
*IL18↓,
*HMGB1↓,
*Casp1↓, shikonin significantly inhibited caspase-1 activation triggered by stimulation with ATP
*NLRP3↓, pharmacologic inhibition of PKM2 by shikonin selectively suppresses NLRP3 and AIM2 inflammasome activation.
*AIM2↓,
*p‑eIF2α↓, Shikonin inhibited EIF2AK2 phosphorylation (Fig. 6a) and caspase-1 activity (Fig. 6b) in PMs obtained from mice subjected to lethal endotoxemia or polymicrobial sepsis.
*Sepsis↓,

4742- SSE,    Antitumor Effects of Selenium
- Review, Var, NA - Review, Arthritis, NA - Review, Sepsis, NA
*antiOx↓, Functions of selenium are diverse as antioxidant, anti-inflammation, increased immunity, reduced cancer incidence, blocking tumor invasion and metastasis, and further clinical application as treatment with radiation and chemotherapy.
*Inflam↓,
Risk↓,
TumCI↓,
TumMeta↓,
radioP↑,
chemoP↑,
Apoptosis↑, (SeDG), which induces cytotoxicity as cell apoptosis, ROS production, DNA damage, and adenosine-methionine methylation in the cellular nucleus
ROS↑,
DNAdam↑,
Dose↑, In our study, advanced cancer patients can tolerate until 5000 μg of sodium selenite in combination with radiation and chemotherapy since the half-life of sodium selenite may be relatively short
selectivity↑, selenium may accumulates more in cancer cells than that of normal cells, which may be toxic to the cancer cells.
*other↓, Se-methylselenocysteine (MSeC) is most abundant in garlic, broccoli, walnut, and some other plant products.
*BioAv↑, Most Se compounds are readily absorbed from the diet and are mainly metabolized in the liver.
ROS↑, Methylselenol induced apoptosis by ROS production, subsequently altered mitochondrial membrane potential, and, further, induced caspases’ activity.
MMP↓,
Casp↑,
*Imm↑, Se activates immune functions via the activation of IL-2 receptor [59].
*Pain↓, Supplementation with 200 μg Se in a group of rheumatoid arthritis patients for three months significantly reduced pain and joint involvement
Sepsis↓, Se plays an important role in defense against acute illness, such as sepsis syndrome
MMP2↓, Several experiments by our group demonstrate that selenite inhibits tumor invasion by blocking MMP-2 and -9 expression
MMP9↓,
*Half-Life↓, a short half-life of sodium selenite and more accumulation of the Se in the cancer cells may be more toxic in cancer cells than that in normal cells.

5024- TQ,    Thymoquinone: A Tie-Breaker in SARS-CoV2-Infected Cancer Patients?
- Review, Covid, NA
*NRF2↑, TQ on Nrf2; it activates Nrf2 by phosphorylation,
*NF-kB↓, results in the reduction of NF-kB, cytokine production, inflammation, oxidative damage and an increase in detoxifying cytoprotective genes and enzymes such as the HO-1 enzyme.
*Inflam↓,
*ROS↓,
*HO-1↑,
antiOx↑, TQ happens to demonstrate potent antioxidant properties, where it significantly attenuates glutathione (GSH) depletion and increases the activity of the glutathione-S-transferase (GST) enzyme.
GSH↑,
GSTs↑,
GSR↑, TQ induces the expression of several detoxifying enzymes, including glutathione reductase, superoxide dismutase 1 (SOD1), catalase, and glutathione peroxidase 2 (GPX)
SOD1↑,
Catalase↑,
GPx↑,
p62↓, TQ significantly decreased P62 and increased expression of beclin1 in CLP mice, thus decreasing sepsis-induced cardiac damage.
Beclin-1↑,
Sepsis↓,
cardioP↑,
hepatoP↑, TQ shows several promising hepatoprotective effects
neuroP↑, TQ shows several neuroprotective effects, as summarized in Table 4

1220- VitC,  VitB1/Thiamine,    The Effect of Thiamine, Ascorbic Acid, and the Combination of Them on the Levels of Matrix Metalloproteinase-9 (MMP-9) and Tissue Inhibitor of Matrix Metalloproteinase-1 (TIMP-1) in Sepsis Patients
- Trial, Sepsis, NA
MMP9:TIMP1↑, highest MMP-9/TIMP-1 ratio was in septic patients receiving thiamine
Sepsis↓, The benefits of ascorbic acid and thiamine in sepsis management have been widely studied.


Showing Research Papers: 1 to 25 of 25

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 25

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   Ferroptosis↑, 1,   GPx↑, 1,   GPx4↓, 1,   GSH↑, 1,   GSR↑, 1,   GSTs↑, 1,   ROS↓, 1,   ROS↑, 5,   SOD↓, 1,   SOD1↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACSL4↑, 1,   AMPK↑, 1,   Glycolysis↓, 1,   PKM2↓, 1,   SIRT1↑, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 2,   Apoptosis↑, 2,   Casp↑, 1,   Cyt‑c↑, 1,   Ferroptosis↑, 1,   GSDMD↑, 1,   JNK↓, 1,   MAPK↓, 1,   Pyro↑, 1,  

Transcription & Epigenetics ⓘ

pRB↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   p62↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   P21↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   CSCs↓, 1,   EMT↓, 2,   ERK↓, 1,   HDAC1↓, 1,   HDAC8↓, 1,   mTOR↓, 1,   PI3K↓, 2,   TumCG↓, 2,   Wnt↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   MMP2↓, 2,   MMP9↓, 3,   MMP9:TIMP1↑, 1,   Smad1↑, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 1,   TumMeta↓, 2,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   LOX1↓, 1,   VEGF↑, 1,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   ICAM-1↓, 1,   Imm↑, 1,   MCP1↓, 1,   NF-kB↓, 4,   PD-L1↓, 1,   PGE2↓, 1,  

Protein Aggregation ⓘ

NLRP3↑, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   BioAv↝, 2,   ChemoSen↑, 2,   Dose↑, 1,   Dose↝, 1,   eff↑, 5,   eff↝, 1,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

PD-L1↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 4,   cardioP↑, 1,   chemoP↑, 3,   hepatoP↑, 1,   neuroP↑, 1,   radioP↑, 1,   Risk↓, 1,   toxicity↝, 2,  

Infection & Microbiome ⓘ

Sepsis↓, 7,  
Total Targets: 93

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 8,   Catalase↑, 6,   Ferroptosis↓, 2,   GPx↓, 1,   GPx1↑, 1,   GPx4↑, 1,   GSH↑, 3,   HNE↓, 1,   HO-1↑, 6,   lipid-P↓, 1,   MDA↓, 5,   MPO↓, 1,   MPO↑, 1,   NOX4↓, 1,   NQO1↑, 1,   NRF2↑, 7,   ROS↓, 14,   mt-ROS↓, 1,   SIRT3↑, 1,   SOD↑, 8,   TAC↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 2,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   mitResp↑, 1,   MMP↑, 1,   OCR↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 2,   AMPK↑, 3,   BUN↓, 1,   ECAR↓, 1,   FAO↑, 1,   FASN↓, 1,   LDH↓, 1,   LDHA↓, 1,   LDL↓, 1,   NADPH↓, 4,   PGM1?, 1,   PKM2↓, 4,   SIRT1↓, 1,   SIRT1↑, 3,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 1,   ASK1↓, 1,   Casp1↓, 1,   Ferroptosis↓, 2,   JNK↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 2,   other↝, 2,  

Protein Folding & ER Stress ⓘ

ATF6↓, 1,   CHOP↓, 1,   p‑eIF2α↓, 1,   ER Stress↓, 2,   GRP78/BiP↓, 4,   IRE1↓, 3,   PERK↓, 2,  

Proliferation, Differentiation & Cell State ⓘ

FOXO3↑, 1,   mTOR↓, 1,   p‑mTOR↓, 1,   PTEN↓, 1,  

Migration ⓘ

AntiAg↑, 1,   MMP9↓, 1,   PKA↑, 1,   TGF-β↓, 1,   α-SMA↓, 2,  

Angiogenesis & Vasculature ⓘ

ATF4↓, 1,   NO↓, 1,   PDI↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

AIM2↓, 1,   COX2↓, 3,   HMGB1↓, 3,   IFN-γ↑, 1,   IL10↓, 1,   IL18↓, 1,   IL1β↓, 6,   IL2↓, 1,   IL5↓, 1,   IL6↓, 7,   IL8↓, 1,   Imm↑, 1,   Inflam↓, 16,   NF-kB↓, 6,   PGE2↓, 1,   TLR2↓, 1,   TLR4↓, 2,   TNF-α↓, 6,  

Synaptic & Neurotransmission ⓘ

GABA↝, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,   NLRP3↓, 5,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

ALAT↓, 2,   AST↓, 2,   creat↓, 1,   IL6↓, 7,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   cardioP↑, 1,   chemoP↑, 1,   cognitive↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 3,   Pain↓, 1,   RenoP↑, 2,   toxicity↓, 3,  

Infection & Microbiome ⓘ

Bacteria↓, 1,   Sepsis↓, 18,  
Total Targets: 111

Scientific Paper Hit Count for: Sepsis, Sepsis
5 Hydrogen Gas
3 Quercetin
3 Rosmarinic acid
2 Capsaicin
1 Alpha-Lipoic-Acid
1 Baicalein
1 Baicalin
1 Betulinic acid
1 Carnosine
1 Disulfiram
1 immunotherapy
1 Propolis -bee glue
1 Psoralidin
1 Cisplatin
1 Selenium NanoParticles
1 Silver-NanoParticles
1 Shikonin
1 Selenite (Sodium)
1 Thymoquinone
1 Vitamin C (Ascorbic Acid)
1 Vitamin B1/Thiamine
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#:1264  State#:%  Dir#:1
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