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Keywords {🔍}

pubmed, article, google, scholar, cas, liver, central, inflammasome, stress, nlrp, wang, disease, hydrogen, fatty, sulfide, nonalcoholic, endoplasmic, reticulum, zhang, chen, nafld, cell, liu, yang, role, pathway, mol, int, sci, exogenous, pyroptosis, activation, inhibiting, inflammation, apoptosis, guo, zhao, med, biol, lipid, access, pharmacol, death, attenuates, autophagy, manuscript, mice, front, hepatic, han,

Topics {✒️}

mir-28a-5p/march7/nlrp3 axis-mediated pyroptosis mt2/camp/pka/ire1 signaling pathway month download article/chapter fasting-induced hepatic steatosis high glucose-induced apoptosis txnip-nlrp3 inflammasome activation high-fat diet er stress/nlrp3 inflammasome nlrp3/nf-κb pathway reactive oxygen species stat3/hif-1alpha pathway sirt1/foxo1/pcsk9 pathway /extracellular signal-regulated kinases endoplasmic reticulum stress nucleotide-binding oligomerization domain ppar-γ signaling liver fibrosis inflammasome ros/thioredoxin-interacting protein h2s-mediated blockage nlrp3 inflammasome prevents cellular biochemistry aims hydrogen sulfide plays hydrogen sulfide-donors full article pdf downregulated endoplasmic reticulum mouse model induced inhibiting er stress influencing nlrp3 inflammasome hydrogen sulfide regulation related subjects privacy choices/manage cookies suppressing lipid accumulation downregulating er stress reducing er stress er stress activates rapamycin signaling pathway activate nlrp3 inflammasomes microvascular endothelial dysfunction regulating nlrp3 inflammasome inflammation prevents nash ameliorates liver injury mtorc2-akt-acly ros/txnip pathways yuhang chen conducted hydrogen sulfide ying li wrote neuronal cell death biol open nox4/ros pathway sd rats liver

Questions {❓}

• Geng Y, Faber KN, de Meijer VE, Blokzijl H, Moshage H (2021) How does hepatic lipid accumulation lead to lipotoxicity in non-alcoholic fatty liver disease?

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         headline:Exogenous hydrogen sulfide improves non-alcoholic fatty liver disease by inhibiting endoplasmic reticulum stress/NLRP3 inflammasome pathway
         description:Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease worldwide, and its exact pathogenesis has not been fully studied. Hydrogen sulfide (H2S) is the third gas signaling molecule discovered in mammals, following nitric oxide and carbon monoxide. It has the effects of anti-inflammation, anti-apoptosis, and so on, thereby playing an important role in many diseases. However, the role and mechanism of exogenous H2S in NAFLD are not fully understood. In this study, we constructed in vitro and in vivo NAFLD models by feeding mice a high-fat diet and stimulating hepatocytes with palmitic acid, respectively, to investigate the improvement effect and mechanism of exogenous H2S on NAFLD. The results showed that NaHS (a donor of H2S) treatment alleviated lipid accumulation, inflammation, apoptosis and pyroptosis, and downregulated endoplasmic reticulum (ER) stress and nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NRRP3) inflammasome in NAFLD. The activation of NLRP3 inflammasome weakened NaHS improvement of NAFLD, indicating that exogenous H2S ameliorated NAFLD by inhibiting NLRP3 inflammasome-mediated lipid synthesis, inflammation, apoptosis and pyroptosis. Similarly, the activation of ER stress weakened NaHS improvement of NAFLD and NaHS inhibition of NLRP3 inflammasome, indicating that exogenous H2S suppressed NLRP3 inflammasome by downregulating ER stress, thus improving NAFLD. Additionally, the protein expressions of NLRP3 and cleaved caspase-1 were downregulated after inhibiting the reactive oxygen species (ROS)/extracellular signal-regulated kinases (ERK) and ROS/thioredoxin-interacting protein (TXNIP) pathways, indicating that ER stress activated NLRP3 inflammasome through the ROS/ERK and ROS/TXNIP pathways. In conclusion, our results indicated that exogenous H2S inhibited NLRP3 inflammasome-mediated hepatocytes inflammation, lipid synthesis, apoptosis and pyroptosis by downregulating ER stress, thereby improving NAFLD; Furthermore, ER stress activated NLRP3 inflammasome through the ROS/ERK and ROS/TXNIP pathways in NAFLD. ER stress/NLRP3 inflammasome is expected to become a new target of H2S for treating NAFLD.
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      description:Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease worldwide, and its exact pathogenesis has not been fully studied. Hydrogen sulfide (H2S) is the third gas signaling molecule discovered in mammals, following nitric oxide and carbon monoxide. It has the effects of anti-inflammation, anti-apoptosis, and so on, thereby playing an important role in many diseases. However, the role and mechanism of exogenous H2S in NAFLD are not fully understood. In this study, we constructed in vitro and in vivo NAFLD models by feeding mice a high-fat diet and stimulating hepatocytes with palmitic acid, respectively, to investigate the improvement effect and mechanism of exogenous H2S on NAFLD. The results showed that NaHS (a donor of H2S) treatment alleviated lipid accumulation, inflammation, apoptosis and pyroptosis, and downregulated endoplasmic reticulum (ER) stress and nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NRRP3) inflammasome in NAFLD. The activation of NLRP3 inflammasome weakened NaHS improvement of NAFLD, indicating that exogenous H2S ameliorated NAFLD by inhibiting NLRP3 inflammasome-mediated lipid synthesis, inflammation, apoptosis and pyroptosis. Similarly, the activation of ER stress weakened NaHS improvement of NAFLD and NaHS inhibition of NLRP3 inflammasome, indicating that exogenous H2S suppressed NLRP3 inflammasome by downregulating ER stress, thus improving NAFLD. Additionally, the protein expressions of NLRP3 and cleaved caspase-1 were downregulated after inhibiting the reactive oxygen species (ROS)/extracellular signal-regulated kinases (ERK) and ROS/thioredoxin-interacting protein (TXNIP) pathways, indicating that ER stress activated NLRP3 inflammasome through the ROS/ERK and ROS/TXNIP pathways. In conclusion, our results indicated that exogenous H2S inhibited NLRP3 inflammasome-mediated hepatocytes inflammation, lipid synthesis, apoptosis and pyroptosis by downregulating ER stress, thereby improving NAFLD; Furthermore, ER stress activated NLRP3 inflammasome through the ROS/ERK and ROS/TXNIP pathways in NAFLD. ER stress/NLRP3 inflammasome is expected to become a new target of H2S for treating NAFLD.
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         Endoplasmic reticulum stress
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         Cancer Research
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