ArticleOxidative medicine and cellular longevity2025
Sotagliflozin Modulation of SIRT1/Nrf2 and PI3K/AKT Signaling Pathway Ameliorates Experimental Liver Fibrosis in Rats.
Article in Oxidative medicine and cellular longevity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Histidine, carnosine, and ergothioneine attenuate pyrazole/LPS-induced hepatotoxicity through modulation of CYP2E1, Nrf2, and NF-κB signaling in mice.Molecular biology reports · 2026Article
- Naringenin attenuates amiodarone-induced pulmonary fibrosis in rats via modulation of the SIRT1/NF-κB signalling pathway.Molecular biology reports · 2026Article
- Sotagliflozin Modulation of SIRT1/Nrf2 and PI3K/AKT Signaling Pathway Ameliorates Experimental Liver Fibrosis in Rats.Oxidative medicine and cellular longevity · 2025Article
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Authors and funding
10 authors.
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Abstract
Background and Purpose: Liver fibrosis poses a major global health burden, contributing substantially to morbidity and mortality worldwide. This study aims to assess the potential novel mechanisms behind the anti-fibrotic effects of sotagliflozin (Sota) in thioacetamide (TAA)-induced liver fibrosis in rats. Experimental Approach: To induce liver fibrosis in rats, 100 mg/kg of TAA was injected intraperitoneally triweekly for 6 weeks. Treated groups were orally administered sotagliflozin (10 and 20 mg/kg) for 4 weeks, concurrent with TAA injections. Key Results: Alongside the histological alterations, the elevation of liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST), lipid profiles total cholesterol (TC) and triglycerides (TAG), cytokines tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), apoptotic markers (caspase-3 and Bcl2 associated X protein [Bax] BAX), phosphatidylinositol 3-kinase (PI3K), phosphorylated protein kinase B (p-AKT), and the lipid peroxidation marker malondialdehyde (MDA) indicated liver dysfunction induced by TAA. Furthermore, indicators of liver fibrosis encompassed reduced levels of albumin, antioxidants; glutathione (GSH), superoxide dismutase (SOD), heme oxygenase-1 (HO-1), and nuclear factor erythroid 2-related factor 2 (Nrf2), antiapoptotic protein B-cell lymphoma-2 (BCL2), sirtuin-1 (SIRT1) expression, and histopathological alterations. Conclusion and Implications: This study demonstrated that daily oral treatment with sotagliflozin markedly upregulated antioxidant markers such as SIRT1 and Nrf2, attenuated TNF-α, and reduced apoptotic and fibrogenic markers, thereby protecting against TAA-induced liver fibrosis. This may have occurred through the augmentation of SIRT1/Nrf2 expression, the inhibition of PI3K/AKT, resulting in the suppression of apoptosis and inflammation.
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