Naringin from Ganshuang granule inhibits inflammatory to relieve liver fibrosis through TGF-β-Smad signaling pathway

• DOI: 10.1371/journal.pone.0304185
• Publication Date: 2024-06-10T17:33:51Z
• Authors: Fuchun Wang; Jian Gan; Rui Li; Rui Yang; Xiaorong Mao; Shuang Liu; Yu Chen; Zhongping Duan; Junfeng Li
• Keywords: Hepatic fibrosis; Granule (geology); Naringin

Objective The present study aims to investigate the specific protective effects and underlying mechanisms of Ganshuang granule (GSG) on dimethylnitrosamine (DMN)-induced hepatic fibrosis in rat models. Methods Hepatic was experimentally evoked rats by DMN administration, varying dosages GSG were employed as an intervention. Hepatocellular damage assessed measuring serum levels aminotransferase bilirubin, accompanied histopathological examinations tissue. concentrations platelet-derived growth factor (PDGF) transforming factor-β1 (TGF-β1) quantitated via enzyme-linked immunosorbent assay (ELISA). expression α-smooth muscle actin (α-SMA) within tissue evaluated using immunohistochemical techniques. interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), a spectrum interleukins (IL-2, IL-4, IL-6, IL-10) quantified quantitative real-time PCR (qRT-PCR). Additionally, stellate cells (HSCs) cultured vitro exposed TNF-α presence naringin, principal component GSG. gene inhibitor metalloproteinase-1 (TIMP-1) matrix metallopeptidase-1 (MMP-1) these also qRT-PCR. Proliferative activity HSCs Cell Counting Kit-8 assay. Finally, alterations Smad protein analyzed through Western blotting. Results Administration with resulted reduced aminotransferases along alleviation liver injury. Furthermore, treated exhibited significant downregulation TGF-β1, PDGF, levels. treatment led increased mRNA IFN-γ, IL-2, well decreased α-SMA liver. pivotal extract GSG, elevated MMP-1 TIMP-1 TNF-α-stimulated when compared control group. naringin administration reduction HSCs. Conclusion has potential mitigate induced models regulation inflammatory factors. Notably, primary may exert role modulating TGF-β-Smad signaling pathway.