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  • Title: Gentiopicroside ameliorates CCl4-induced liver injury in mice by regulating the PPAR-γ/Nrf2 and NF-κB/IκB signaling pathways.
    Author: Zhang Y, Pan S, Yi S, Sun J, Wang H.
    Journal: J Int Med Res; 2023 Oct; 51(10):3000605231204501. PubMed ID: 37802492.
    Abstract:
    OBJECTIVE: This study explored the mechanisms by which gentiopicroside protects against carbon tetrachloride (CCl4)-induced liver injury. METHODS: Male mice were randomly assigned to the control; CCl4; bifendate 100 mg/kg; or gentiopicroside 25, 50, or 100 mg/kg groups. Both vehicle and drugs were administered intragastrically for 7 days. Mice were administered CCl4 intraperitoneally 1 hour after the last drug dose. After 24 hours, we collected blood and liver samples for testing. RESULTS: Gentiopicroside significantly reduced serum alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase activities with corresponding reductions in hepatocyte denaturation and necrosis. Gentiopicroside enhanced superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and glutathione levels and reduced heme oxygenase 1 (HO-1) activity and malondialdehyde levels in the liver, and these effects were attributed to peroxisome proliferator-activated receptor (PPAR)-γ/nuclear factor erythroid 2-related factor 2 (Nrf2) activation. Meanwhile, gentiopicroside significantly downregulated HO-1 and upregulated SOD and GSH-Px at the mRNA level in the liver. Furthermore, gentiopicroside significantly suppressed serum tumor necrosis factor-α and interleukin-1β secretion, which was associated with the inhibition of nuclear factor-kappa B (NF-κB)/inhibitor of NF-κB (IκB). CONCLUSIONS: Gentiopicroside ameliorated CCl4-induced liver injury in mice via the PPAR-γ/Nrf2 and NF-κB/IκB pathways.
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