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Catalpol attenuates hepatic glucose metabolism disorder and oxidative stress in triptolide-induced liver injury by regulating the SIRT1/HIF-1α pathway

Weijue Nie, Hong Zhu, Xin Sun, Jie Zhou, Heng Xu, Zhichao Yu, Minghao Lu, Baoping Jiang, Lingling Zhou, Xueping Zhou

2024International Journal of Biological Sciences29 citationsDOIOpen Access PDF

Abstract

knockout models, we confirmed SIRT1 as a mechanism of action for CAT. Our findings revealed that CAT could alleviate TP-induced liver injury by activating SIRT1, which inhibited lysine acetylation of hypoxia-inducible factor-1α (HIF-1α), thereby restoring the balance between glycolysis and oxidative phosphorylation. This action improved mitochondrial dysfunction and reduced glucose metabolism disorder and oxidative stress caused by TP. Taken together, these insights unveil a hitherto undocumented mechanism by which CAT ameliorates TP-induced liver injury, positioning it as a potential therapeutic agent for managing TP-induced hepatotoxicity.

Topics & Concepts

Oxidative stressCatalpolTriptolideLiver injuryMetabolismPharmacologyCarbohydrate metabolismChemistryLiver damageMedicineBiochemistryEndocrinologyApoptosisGlycosideOrganic chemistryNatural Compounds in Disease TreatmentPharmacological Effects and Toxicity StudiesDrug-Induced Hepatotoxicity and Protection
Catalpol attenuates hepatic glucose metabolism disorder and oxidative stress in triptolide-induced liver injury by regulating the SIRT1/HIF-1α pathway | Litcius