Sepsis Cancer Research Results

Sepsis, Sepsis: Click to Expand ⟱

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Type:

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,

*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,

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/PTGS2↓, 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,

Review,

Stroke,

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/CCL2↓,
MMP9↓,
COX2/PTGS2↓, 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,

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/PTGS2↓, 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,

Warburg↓, Capsaicin inhibits the Warburg effect by binding directly to Cys424 residue and LDHA of pyruvate kinase isoenzyme type M2 (PKM2).
*PKM2↓,
*COX2/PTGS2↓, 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,

Review,

Stroke,

*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/KDR/Flk1↓,
NF-kB↓, suppressing nuclear factor kB (NF-κB) signaling pathway activation in human colon cancer cells

6650-

Cen,

Therapeutic Potential of Centella asiatica and Its Triterpenes: A Review

Review,

AD,

*BioAv↝, madecassoside, asiaticoside, madecassic acid, and asiatic acid are widely distributed in the body and madecassoside, asiaticoside may exert their biological activity through converted into aglycone (madecassic acid, and asiatic acid).
*BioAv↝, C. asiatica enhances the function of the nervous system. It dissolves in methanol, ethanol, and water.
*MDA↓, Male Wistar rats – MDA ↓, GSH ↑, SOD ↑, AChE↓
*GSH↑,
*SOD↑,
*AChE↓,
*memory↑, Male SD rats; hippocampal cell – Spatial working memory↑, Ki-67 cells↑
*Ki-67↑,
*Catalase↑, Male SD rats MAPK SOD↑, LPO↑, CAT↑, GSH↑, dopamine↑, glutamate↑, Syn1↑, Stx1A↑, PI3K↑, PDK1↑, PEBP↓, VMAT2↑, TH ↑, MAPK ↑, BDNF↑, NGF↑
*PI3K↑,
*BDNF↑,
*NGF↑,
*ROS↓, Water extract of CA Tg2576 mice – ROS↓, NRF2↑, GCLC↑, HMOX1↑, NQO1↑, ATP↑, Mt-ND1↑, Mt-ATP6↑, Mt-CO1↑, Mt-CYB↑, oxygen consumption rate↑
*NRF2↑,
*HO-1↑,
*NQO1↑,
*ATP↑,
*OCR↑,
*TNF-α↓, Ethanolic extract of CA Male SD rats – TNF-α↓, BDNF↑
*PP2A↑, Ethanolic extract of CA Male albino Wistar rats PP2A/GSK-3B PP2A↑, GSK-3B↓, Bcl-2↑
*GSK‐3β↓,
*Bcl-2↑,
*TrkB↑, Standardized extract of CA Male Wistar rats – NR2A↑, NR2B↑, BDNF↑,TrkB↑
*NOTCH1↑, Asiatic acid Male SD rats – Notch1↑, SOX2↑, DCX↑, Nrf2↑, nestin↑, p21 positive cells↓, MDA↓
*SOX2↑,
*Nestin↑,
*MDA↓,
*MAOA↓, Asiaticoside-D Worms – MAO-A↓, MAO-B↓
*MAOB↓,
*GPx↑, Previous studies found that C. asiatica and its triterpenoids could effectively increase SOD and GPX activities, activate nuclear factor erythroid-2-related factor 2, improve the cognitive impairment of animals,
*cognitive↑,
*ROS↓, C. asiatica and its triterpenoids could reduce ROS production
*neuroP↑, they reduced related nerve cell apoptosis, increased synaptic density, and improved the survival rate of neural cells
*glucose↓, Methanol extract of CA Male SD rats – Blood glucose ↓, food and water intake ↓, ALT↓, AST↓, PFK ↑, GS ↑, GP↑, glycogen content ↑
*ALAT↓,
*AST↓,
*PFK↓,
*Weight↓, inhibit weight gain
*Inflam↓, (4) ameliorate inflammation,
*AntiDiabetic↑, C. asiatica extract and related components (asiatic acid, madecassoside) for the treatment of endocrine diseases such as diabetes, obesity and osteoporosis are excellent.
*Obesity↓,
*Wound Healing↑, The C. asiatica extract and its triterpenoids had certain therapeutic and relieving effects on acne, baldness, vitiligo, atopic dermatitis, and wounds. C. asiatica extract can effectively promote wound healing in diabetic patients
*cardioP↑, C. asiatica has a positive effect on cardiovascular diseases.
*GutMicro↑, C. asiatica and its triterpenoids also have therapeutic effects on digestive disorders, which is mainly reflected by improved liver fibrosis, colitis, and gastric mucosal damage; and even reduced Helicobacter pylori gastric colonization
*Sepsis↓, Asiatic acid can improve the side effects caused by antibiotics, reverse multidrug resistance (MDR), and reduce sepsis.
*BioAv↑, C. asiatica cream containing 5.12% asiaticoside and 5.1% madecassoside can be completely absorbed by the skin and effectively improve pigmentation and may be used in treating hypertrophic scars

6421-

CUR,

Curcumin simultaneously improves mitochondrial dynamics and myocardial cell bioenergy after sepsis via the SIRT1-DRP1/PGC-1α pathway

in-vivo,

Nor,

orally once daily at a volume of 4 mL/kg body weight

Male C57BL/6J wild-type mice

*SIRT1↓, Curcumin activated sirtuin 1 (SIRT1); increased expression of the mitochondrial biogenesis-related genes Pgc1α, Tfam, and Nrf2; reduced dynamin-related protein 1 translocation from the cytoplasm to mitochondria;
*PGC-1α↑,
*NRF2↑,
*DRP1/DNM1L↓,
*Sepsis↓, Curcumin improves survival of sepsis model mice by protecting cardiac function
*OS↑,
*cardioP↑,

6282-

DL,

Limonene Exerts Anti-Inflammatory Effect on LPS-Induced Jejunal Injury in Mice by Inhibiting NF-κB/AP-1 Pathway

in-vivo,

IBD,

Oral administration of limonene at dosages of 100 and 200 mg/kg was used in the LPS mouse model.

mouse

*RenoP↑, pretreatment with limonene at doses of 100 and 200 mg/kg mitigated this decline in renal function, evidenced from the reduced levels of serum urea and creatinine.
*creat↓,
*Inflam↓, Limonene demonstrated anti-inflammatory effects by reducing pro-inflammatory cytokines (TNF-α, IL-1β, COX-2), suppressing the TLR4/NF-κB/AP-1
*TNF-α↓,
*IL1β↓,
*COX2/PTGS2↓,
*ROS↓, modulating oxidative stress through Nrf2 activation.
*NRF2↑,
*GastroP↑, mitigating intestinal inflammation and preserving gastrointestinal health.
*TLR4↓, suppressing the TLR4/NF-κB/AP-1
*NF-kB↓,
*AP-1↓,
*Sepsis↓, limonene has the potential to mitigate the severity of sepsis in mice.

4914-

DSF,

immuno,

Disulfiram and cancer immunotherapy: Advanced nano-delivery systems and potential therapeutic strategies

Review,

Var,

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/ABCB1↓, 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,

7228-

EGb 761,

Current Perspectives on the Beneficial Role of Ginkgo biloba in Neurological and Cerebrovascular Disorders

Review,

AD,

*Dose↝, A standardized formulation, EGb 761®, also sold as Tanakan® or Tebonin®, was created to normalize the constituents to assure reliable and consistent drug performance and the absence of ginkgolic acid, a known allergen naturally found in Ginkgo
*PAF↑, Ginkgolides have been clinically shown to act as platelet-activating factor (PAF) antagonists, inhibiting platelet aggregation and promoting increased blood flow.
*AntiAg↑,
*BloodF↑,
*Inflam↓, Additionally, BB(bilobalide) has shown anti-inflammatory properties and neuroprotection in preclinical models of stroke16 and AD
*neuroP↑,
*Stroke↓, Alternatively, promising results have been observed that support administration of EGb 761 soon after the onset of ischemia and during the recovery period.
*Dose↝, The standard clinical dose of EGb 761 is 120 mg (~1.7 mg/kg) once or twice daily; thus, a standard dose will contain ~3–4 mg ginkgolides A, B, and C, 3–4 mg BB, and 29 mg flavonoids.
*Sepsis↓, Patients treated with antimicrobials plus GB showed a significant drop in mortality as compared to patients treated with antimicrobials and placebo; this finding led to the development of other PAF antagonists for the treatment of sepsis
*memory↑, when administered daily, EGb 761 (240 mg daily) may improve some aspects of memory better than others

6877-

FA,

The protective role of ferulic acid on sepsis-induced oxidative damage in Wistar albino rats

in-vivo,

Nor,

Wistar albino rats

*antiOx↑, Ferulic acid (FA), a well-established natural antioxidant, has several pharmacological activities including anti-inflammatory, anticancer and hepatoprotective.
*Inflam↓,
*AntiCan↑,
*hepatoP↑,
*DNAdam↓, DNA damage in sepsis+FA-treated group was significantly lower than the sepsis group.
*Sepsis↓,
*MDA↓, FA treatment also decreased the MDA levels and increased the GSH levels and SOD and GSH-Px activities in the sepsis-induced rats. I
*GSH↑,
*GPx↑,
*ROS↓, It seems that FA might have ameliorative effects against sepsis-induced oxidative damage.

7482-

H2,

Molecular Hydrogen Therapy: Mechanisms, Delivery Methods, Preventive, and Therapeutic Application

Review,

Var,

Review,

IBD,

Review,

Stroke,

Review,

Sepsis,

Review,

AD,

Dose↝, H2 can be administered exogenously and is also produced endogenously within the intestinal tract.
*Inflam↓, Anti‐Inflammatory Effect
*IL1β↓, diabetes combined with stroke, H₂ intervention downregulates the expression levels of proinflammatory factors (IL‐1β, IL‐6, TNF‐α), while activating the TLR4/NF‐κB signaling pathway to achieve neuroprotective effects
*IL6↓,
*TNF-α↓,
*neuroP↑,
*mTOR↓, sepsis model, H₂ regulates macrophage polarization (inhibiting the M1 phenotype/promoting the M2 phenotype) and inhibits (mTOR) phosphorylation, reducing the release of inflammatory mediators such as IL‐6, TNF‐α, and HMG
*IL10↑, while increasing the levels of anti‐inflammatory factors IL‐10 and Transforming Growth Factor‐beta (TGF‐β)
*TGF-β↑,
*Sepsis↓,
*NRF2↑, whereas Nrf2 induction suppresses these pathways via redox homeostasis modulation
*antiOx↑, figure 1
*Catalase↑,
*SOD↑,
*GPx↑,
*ROS↓, H₂ mediates ROS regulation through Nrf2, inhibiting NF‐κB/NLRP3 inflammasome activation and achieving an antioxidant–anti‐inflammatory synergistic effect
*HO-1↑, H2 can increase the expression of heme oxygenase‐1 (HO‐1) or activate the phosphatidylinositol‐3‐kinase (PI3K)–Akt signaling pathway to improve liver I/R injury
*PI3K↑,
*Akt↑,
*hepatoP↑,
*MPO↓, reduce myeloperoxidase (MPO) activity and IL‐1β/TNF‐α levels to alleviate myocardial injury
*cardioP↑,
CDK4↓, Studies have demonstrated that H2 inhibits CDK4 and CDK6 to restrict lung cancer progression
CDK6↑,
CD47↓, H₂ can reverse immune escape in lung cancer cells by inhibiting the expression of CD47 and activating the apoptosis program
PI3K↓, H2 promotes apoptosis by downregulating Akt phosphorylation and inhibiting the PI3K signaling pathway in non‐small cell lung cancer.
Akt↓,
Hif1a↓, inhalation of H2 suppresses Hypoxia‐Inducible Factor 1 Alpha Subunit (HIF‐1α)/NF‐κB signaling pathway activation and promotes apoptosis in HeLa cells
selectivity↑, This bidirectional regulatory capability allows H₂ to protect normal tissues from excessive apoptosis (such as inflammation‐induced cell death) while selectively inducing apoptosis in tumor cells.
*MMP↑, howed that after treating septic rats with HRS, the decline in mitochondrial membrane potential (MMP) and ATP content was improved.
*ATP↑,
*ER Stress↓, H₂ alleviated inflammation and organ damage by inhibiting ER stress and activating the autophagy pathway in septic mice
*CHOP/DDIT3↓, H2 could downregulate the expression of CHOP, caspase‐12, and GRP78, while inhibiting p38 and c‐Jun N‐terminal kinase (JNK) phosphorylation, and upregulating the LC3‐II/I ratio
*Casp12↓,
*GRP78/BiP↓,
*p38↓,
*p‑JNK↓,
*LC3‑Ⅱ/LC3‑Ⅰ↑,
*p‑eIF2α↓, HRW prevents IBD in mice by reducing levels of p‐eIF2α, ATF4, XBP1, and CHOP, key proteins in ER stress.
*ATF4↓,
*XBP-1↓,
*Imm↑, H₂ exhibit multidimensional characteristics, primarily enhancing immunity by protecting immune organs,
*IFN-γ↓, H2 treatment inhibited several T‐cell effector molecules, such as IFN‐γ, IL‐4, and GZMB
*IL4↓,
*GranB/GZMB↓,
NK cell↑, After inhaling H₂ for 2 weeks, patients with advanced non‐small cell lung cancer showed significant improvement in T‐cell exhaustion. (NK) subgroups was higher than the pretreatment percentag
radioP↑, HRS can protect against radiation‐induced immune dysfunction by restoring the number of CD4+ T and CD8+ T cells in the spleen.
*CD4+↑,
CD8+↑,
*Dose↝, Common delivery methods include inhalation, oral administration of HRW, injection of HRS, promotion of endogenous H2 production
*other↑, H2, which fall within the explosive range at concentrations ranging from 4 to 74%, it is essential to specify the concentration of H2 for inhalation therapy.
*Dose↝, China National Health Commission recommends the administration of oxygen–H2 mixture (33.3% O2 and 66.6% H2)
*antiPs↑, HRW baths exhibit inhibitory effects on inflammation and oxidative stress while demonstrating therapeutic benefits for conditions such as psoriasis
*BioAv↝, the solubility of H2 in water at room temperature and pressure is limited to a maximum of 0.8mM109, resulting in limited efficacy when orally administered.
*GutMicro↑, inhalation of H2 modulates the gut flora to ameliorate acute alcoholic liver injury. H2 altered the composition of the GM, leading to an increase in the relative abundance of Mycobacterium anisopliae and Mycobacterium thickum
Dose↝, CRC cell lines (ROK/SW480/HCT116) and xenograft mouse models,Inhalation of 66% H2 (66% H2 and 33% O2);Duration: 2 h a day for 21 days
*IBI↑, orally administered silicon H2 nanoparticles (SiH NPs) for targeted scavenging of ROS at inflammatory sites, thereby alleviating symptoms of IBD and restoring GM diversity by enhancing the abundance of beneficial bacteria.
TumCP↓, H2 inhibits tumor cell activity, proliferation, invasion, and migration through various molecular mechanisms, in a manner that depends on both dose and time.
TumCI↓,
TumCMig↓,
CD8+↑, H2 Improves Prognosis by Restoring Depleted CD8+ T Cells in Patients with CRC Cancer
PGC-1α↑, It has been shown that H2 can activate PGC‐1α to restore mitochondrial function and rescue depleted CD8+T cells
Akt↓, H2 Inhibits CRC Cell Proliferation by Suppressing the AKT/SCD1 Pathway
SCD1↓,
*MDA↓, The results showed that H2 water alone significantly improved detected antioxidant markers (SOD and CAT) and reduced MDA levels.
eff↑, combination of H2 water and 5‐fluorouracil significantly attenuated MDA levels more effectively than 5‐fluorouracil alone
*APP↓, H2 gas significantly inhibited the overexpression of APP, BACE1, and sAP, thereby reducing Aβ production.
*BACE/β-secretase↓,
*Aβ↓,
*cognitive↑, This intervention effectively halted the progression of AD, alleviating cognitive impairment, synaptic deficits, and neuronal death
*neuroP↑, regulation of GM(gutmicrobiome) by HRW considered a key mechanism underlying its neuroprotective effects.
NP/CIPN↓, mice with chemotherapy‐induced neuropathic pain caused by oxaliplatin, drinking HRW significantly reduced inflammation by inhibiting the LPS–TLR4 pathway and decreasing the expression of TNF‐α and IL‐6.
*Stroke↓, inhalation of 2% H2 gas significantly reduced levels of myocardial injury markers, such as creatine kinase‐MB and cardiac troponin‐T, while protecting myocardial tissue from further damage by inhibiting autophagy.
*NLRP3↓, daily inhalation of 2% H2 gas for 3 h over 28 days effectively suppressed the activation of the NLRP3 inflammasome, reduced cardiac fibrosis, and improved cardiac function
*ALAT↓, 4% H2 outperforming 67% H2 in reducing liver enzyme levels Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) and lipid accumulation.
*AST↓,
*LPS↓, inhalation of 4% H2 in an NAFLD rat model significantly lowered plasma LPS levels, inhibited the LPS/TLR4/NF‐κB signaling pathway to reduce liver inflammation
*hepatoP↑, drinking HRW, indicating its hepatoprotective effects
chemoP↑, injecting HRS in rats effectively reduced ALT and AST levels caused by doxorubicin, decreased ROS and MDA production, and regulated the Bax/Bcl‐2 ratio to alleviate inflammation and apoptosis.
*creat↓, mouse model of kidney injury induced by a high‐oxalate diet, HRW consumption markedly improved serum creatinine, blood urea nitrogen, and kidney injury markers such as kidney injury molecule‐1 (KIM‐1)
*Urea↓,
*RenoP↑,
*eff↑, higher concentrations of H2 gas (67%) produced more pronounced improvements in kidney histology and morphology compared with lower concentrations (4%)
Apoptosis↑, H2 gas increased apoptosis in A549 cells while reducing the expression of XIAP and BIRC3 proteins in studies on A549 cells and their nude mouse models.
XIAP↓,
IAP2/BIRC3↓,
TumVol↓, inhalation of 60% H2 gas significantly reduced tumor volume in experimental mice
MALAT1↓, In gastric cancer research, Zhu et al. [10] found that H2 gas downregulated the expression of lncRNA MALAT1 and EZH2 while upregulating miR‐124‐3p
EZH2↓,
miR-124-3p↓,
eff↑, combining platinum nanocolloid (Pt‐nc) with H2 gas effectively inhibited the growth of human promyelocytic leukemia HL60 cells
ChemoSen↑, combining H2 therapy with conventional treatments such as chemotherapy and radiotherapy, demonstrating improved efficacy and reduced side effects
*compII↑, allergic airway inflammation, showing that H2 increased ATP production as well as the activity of mitochondrial respiratory chain complexes I and III
*compIII↑,
*LDL↓, H2‐enriched water in humans, showing that supplementation with H2‐enriched water appeared to reduce serum low‐density lipoprotein cholesterol (LDL‐C) and apolipoprotein B (apoB) levels,
*Obesity↓, H2 may play a beneficial role in the prevention of potential metabolic syndrome
QoL↑, 82 patients with stage III and IV cancers receiving H2 inhalation therapy. They found that H2 inhalation improved the quality of life
PFS↑, Sixteen months of follow‐up found that progression‐free survival in the control group was lower than that in the H2 inhalation group alone, and significantly lower than that in the other three combination therapy groups.

7927-

H2,

Hydrogen gas (XEN) inhalation ameliorates airway inflammation in asthma and COPD patients

Human,

Asthma,

In total, 2.4% hydrogen containing steam mixed gas (XEN) was inhaled once for 45 min in 10 patients with asthma and 10 patients with COPD.

*IL8↓, decreased IL-8 level only in asthma group
*IL4↓, IL-4 and IL-6 levels in EBC were significantly lower after inhalation in the COPD (0.80–0.64 pg/mL, P = 0.025) and asthma (0.06–0.05 pg/mL, P = 0.007) group, respectively.
*IL6↓,
*Inflam↓, A single inhalation of hydrogen for 45 min attenuated inflammatory status in airways in patients with asthma and COPD
*Sepsis↓, has been demonstrated that hydrogen could provide protection against various diseases, including sepsis, stroke and ischemia-reperfusion injury
*Stroke↓,
*antiOx↑, Hydrogen, which exhibits anti-oxidative and anti-inflammation effects, was proved to be relatively safe for inhalation in diving.9
*toxicity↓,

2515-

H2,

Recent Advances in Studies of Molecular Hydrogen against Sepsis

Review,

Sepsis,

*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,

Review,

Sepsis,

*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,

Review,

Park,

*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,

*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,

*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.

7567-

HYP,

Hyperoside: A review on its sources, biological activities, and molecular mechanisms

Review,

Var,

*AntiCan↑, anticancer, anti-inflammatory, antibacterial, antiviral, antidepressant, and organ protective effects.
*Bacteria↓,
*AntiViral↑,
*antiD↓,
*RenoP↑, Kidney protection
*hepatoP↑, Liver protection
*eff↑, treating multiple diseases, such as sepsis, arthritis, colitis, diabetic nephropathy, myocardial ischemia-reperfusion, pulmonary fibrosis, and cancers.
*Sepsis↓,
*AntiArt↑,
*Stroke↓,
TumCMig↓, hyperoside has been shown to inhibit the migration and invasion properties of A549 cells by suppressing the expression of metastasis-associated gene 1 (MTA1), matrix metalloproteinase-2 inhibitor (TIMP-2), matrix metalloproteinase (MMP)-2
TumCI↓,
MTA1↓,
TIMP2↓,
MMP2↓,
MMP↓, disrupted the penetration of the mitochondrial membrane, and triggered mitochondrial cytochrome C and apoptosis inducers into the cytoplasm
Cyt‑c↑,
Akt↓, inhibited the Akt/mTOR/p70S6K signaling pathway in NSCLC cells to promote autophagy and exerted anticancer activity
mTOR↓,
P70S6K↓,
TumAuto↑,
PD-L1↓, thereby inhibiting PD-L1 expression at the transcriptional leve
TNF-α↓, subsequently, inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1b, IL-6 and IL-8, were significantly down-regulated
IL1β↓,
IL6↓,
IL8↓,
Bcl-2↓, Hyperoside was reported to inhibit the over-expression of B-cell lymphoma factor 2 (Bcl)-2 and Bcl-x in lung cancer cells, and up-regulate the preapoptotic factors such as Bax, Bad, and Bak.
Bcl-xL↓,
BAX↑,
BAD↑,
Bak↑,
VEGF↓, decreasing the HeLa cell's vascular endothelial growth factor (VEGF) expression levels in HeLa cells.
Casp3↑, hyperoside promoted apoptosis via enhancing caspase-3 and caspase-8 protein expression, and on the other hand, by promoting tumor suppressor gene P35 expression
Casp8↑,
P53↑,
GSH↓, Hyperoside could also reduce glutathione levels in HeLa cells, superoxide dismutase (SOD), and Catalase (CAT) viability.
SOD↓,
Catalase↓,
TAC↓, reduced the antioxidant capacity and thus to inhibit cancer cell growth
XIAP↓, MCF-7 and 4 T1 cells Decreased the levels of Bcl-2 and XIAP; increased the levels of Bax and cleaved cysteine protease-3; decreased the production of ROS and inhibited NFκB signal pathway
ROS↓,
NF-kB↓,
TLR4↓, MDA-MB-231 cells Inhibited TLR4-NF-κB signaling pathways; decreased the expression of Bcl-2; enhanced the expression of pro-apoptotic Bax and the level of pro-inflammatory cytokine IL-6
P-gp/ABCB1↓, S180 cancer cell Reduced the expression of P-gp, LRP and Bcl-2 and increased the expression of Fas; inhibited bad phosphorylation and increased p27 level
LRP1↓,
Fas↑,
p27/CDKN1B↑,
*cardioP↑, Cardiovascular protection In vivo pulmonary embolism and arterial thrombosis model Prolonged the activated prothrombin time and suppressed thrombin and FXa activities; inhibit the production of PAI-1 induced by TNF-α
*AntiThr↑,
*PAI-1/SERPINE1↓,
*BUN↓, Reduced the contents of serum angiotensin converting enzyme ArgII, ALD, U-mAlb, BUN, SCR, ALT, and AST
*ALAT↓,
*AST↓,
*neuroP?, Neuroprotection

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,

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/PTGS2↓, 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

2.5 to 120 µM)

Xenograft experiments in nude mice

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,

endotoxin-induced ALI mouse model

*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,

rats

*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,

*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/DDIT3↓,
*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,

mice

*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,

*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,

*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,

*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,

mice

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,

Review,

Arthritis,

Review,

Sepsis,

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

5024-

TQ,

Thymoquinone: A Tie-Breaker in SARS-CoV2-Infected Cancer Patients?

Review,

Covid,

*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,

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 33 of 33

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 33

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 2, Sepsis↓, 7,
Total Targets: 134

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AntiArt↑, 1, antiD↓, 1, compII↑, 1, PAF↑, 1, Stroke↓, 4,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1, antiOx↑, 11, Catalase↑, 8, Ferroptosis↓, 2, GPx↓, 1, GPx↑, 3, GPx1↑, 1, GPx4↑, 1, GSH↑, 5, HNE↓, 1, HO-1↑, 8, lipid-P↓, 1, MDA↓, 9, MPO↓, 2, MPO↑, 1, NOX4↓, 1, NQO1↑, 2, NRF2↑, 11, ROS↓, 19, mt-ROS↓, 1, SIRT3↑, 1, SOD↑, 10, TAC↑, 1,

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 2,

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 3, compIII↑, 1, DRP1/DNM1L↓, 1, mitResp↑, 1, MMP↑, 2, OCR↑, 2, PGC-1α↑, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 5, AMPK↑, 3, BUN↓, 2, ECAR↓, 1, FAO↑, 1, FASN↓, 1, glucose↓, 1, LDH↓, 1, LDHA↓, 1, LDL↓, 2, NADPH↓, 4, PFK↓, 1, PGM1?, 1, PKM2↓, 4, SIRT1↓, 2, SIRT1↑, 3, Warburg↓, 1,

Cell Death(tgid=5) ⓘ

Akt↓, 1, Akt↑, 1, ASK1↓, 1, Bcl-2↑, 1, Casp1↓, 1, Casp12↓, 1, Ferroptosis↓, 2, GranB/GZMB↓, 1, JNK↓, 1, p‑JNK↓, 1, p38↓, 1,

Transcription & Epigenetics(tgid=7) ⓘ

AntiThr↑, 1, other↓, 2, other↑, 1, other↝, 2,

Protein Folding & ER Stress(tgid=8) ⓘ

ATF6↓, 1, CHOP/DDIT3↓, 2, p‑eIF2α↓, 2, ER Stress↓, 3, GRP78/BiP↓, 5, IRE1↓, 3, PERK↓, 2, XBP-1↓, 1,

Autophagy & Lysosomes(tgid=9) ⓘ

LC3‑Ⅱ/LC3‑Ⅰ↑, 1,

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,

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

FOXO3↑, 1, GSK‐3β↓, 1, mTOR↓, 2, p‑mTOR↓, 1, Nestin↑, 1, NOTCH1↑, 1, PI3K↑, 2, PTEN↓, 1, SOX2↑, 1,

Migration(tgid=13) ⓘ

AntiAg↑, 2, AP-1↓, 1, APP↓, 1, Ki-67↑, 1, MMP9↓, 1, PAI-1/SERPINE1↓, 1, PKA↑, 1, TGF-β↓, 1, TGF-β↑, 1, α-SMA↓, 2,

Angiogenesis & Vasculature(tgid=14) ⓘ

ATF4↓, 2, NO↓, 1, PDI↓, 1,

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1, GastroP↑, 1, IBI↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

AIM2↓, 1, CD4+↑, 1, COX2/PTGS2↓, 4, HMGB1↓, 3, IFN-γ↓, 1, IFN-γ↑, 1, IL10↓, 1, IL10↑, 1, IL18↓, 1, IL1β↓, 8, IL2↓, 1, IL4↓, 2, IL5↓, 1, IL6↓, 9, IL8↓, 2, Imm↑, 2, Inflam↓, 22, LPS↓, 1, NF-kB↓, 7, PGE2↓, 1, TLR2↓, 1, TLR4↓, 3, TNF-α↓, 9,

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1, BDNF↑, 1, GABA↝, 1, MAOA↓, 1, NGF↑, 1, TrkB↑, 1,

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 2, BACE/β-secretase↓, 1, MAOB↓, 1, NLRP3↓, 6, PP2A↑, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2, BioAv↝, 3, Dose↝, 5, eff↑, 7, Half-Life↓, 1,

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 5, AST↓, 5, BloodF↑, 1, creat↓, 3, GutMicro↑, 2, IL6↓, 9, Ki-67↑, 1, LDH↓, 1, Urea↓, 1,

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1, AntiCan↑, 2, AntiDiabetic↑, 1, antiPs↑, 1, cardioP↑, 5, chemoP↑, 1, cognitive↑, 3, hepatoP↑, 5, memory↑, 3, neuroP?, 1, neuroP↑, 7, Obesity↓, 2, OS↑, 1, Pain↓, 1, RenoP↑, 5, toxicity↓, 4, Weight↓, 1, Wound Healing↑, 1,

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1, Bacteria↓, 2, Sepsis↓, 26,
Total Targets: 172

Scientific Paper Hit Count for: Sepsis, Sepsis

7 Hydrogen Gas
3 Quercetin
3 Rosmarinic acid
2 Capsaicin
1 Alpha-Lipoic-Acid
1 Baicalein
1 Baicalin
1 Betulinic acid
1 Carnosine
1 Centella asiatica / Gotu kola → asiaticoside
1 Curcumin
1 D-limonene
1 Disulfiram
1 immunotherapy
1 Ginkgo biloba-EGb 761
1 Ferulic acid
1 Hyperoside
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
  wNotes=on  sortOrder:rid,rpid

Sepsis Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Protein Aggregation(tgid=19) ⓘ

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Metal & Cofactor Biology(tgid=2) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Protein Aggregation(tgid=19) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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