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<p>Hepatic fibrosis was induced in Swiss albino mice by intraperitoneal administration of CCl<sub>4</sub> (1 mL/kg, twice weekly) for 8 weeks, followed by oral treatment with <i>Glycosmis pentaphylla</i> methanolic extract (GPME) at 200 or 400&#xa0;mg/kg/day or silymarin (50&#xa0;mg/kg/day) for 4 weeks. GPME treatment dose-dependently restored liver function by significantly reducing elevated serum ALT, AST, and ALP levels, ameliorated histological damage with decreased collagen deposition and preserved hepatocyte ultrastructure as evidenced by H&amp;E staining, IHC, TEM, and SEM, and lowered hepatic hydroxyproline content. It further modulated inflammatory responses by upregulating anti-inflammatory IL-10 while downregulating pro-inflammatory and pro-fibrotic cytokines TGF-β, TNF-α, and IL-6, and attenuated oxidative stress by enhancing SOD, CAT, and GSH activities while reducing MDA levels. Western blot and IHC analyses confirmed suppression of TGF-β, α-SMA expression, and Smad2/3 phosphorylation. GC-MS and LC-MS profiling identified 37 bioactive compounds, of which three leads exhibited strong binding affinities (-7.2 to -8.2&#xa0;kcal/mol) to TGFβR1 in molecular docking studies. Collectively, these findings demonstrate that GPME effectively mitigates CCl<sub>4</sub>-induced hepatic fibrosis through inhibition of TGF-β/Smad signaling, reduction of oxidative stress, and modulation of inflammatory responses, supporting its potential as a natural anti-fibrotic agent.</p>

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Glycosmis pentaphylla mitigates CCl4-induced hepatic fibrosis in Swiss albino murine model through suppression of TGF-β/Smad2/3 signaling, oxidative stress and inflammatory responses: in-vivo and in-silico approach

  • 期刊论文

  • 发表日期：

    2026年3月10日

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  • Madhubanti Das,
  • Nabanita Baruah,
  • Jogen Chandra Kalita,
  • Kandarpa Kumar Saikia

摘要

Hepatic fibrosis was induced in Swiss albino mice by intraperitoneal administration of CCl4 (1 mL/kg, twice weekly) for 8 weeks, followed by oral treatment with Glycosmis pentaphylla methanolic extract (GPME) at 200 or 400 mg/kg/day or silymarin (50 mg/kg/day) for 4 weeks. GPME treatment dose-dependently restored liver function by significantly reducing elevated serum ALT, AST, and ALP levels, ameliorated histological damage with decreased collagen deposition and preserved hepatocyte ultrastructure as evidenced by H&E staining, IHC, TEM, and SEM, and lowered hepatic hydroxyproline content. It further modulated inflammatory responses by upregulating anti-inflammatory IL-10 while downregulating pro-inflammatory and pro-fibrotic cytokines TGF-β, TNF-α, and IL-6, and attenuated oxidative stress by enhancing SOD, CAT, and GSH activities while reducing MDA levels. Western blot and IHC analyses confirmed suppression of TGF-β, α-SMA expression, and Smad2/3 phosphorylation. GC-MS and LC-MS profiling identified 37 bioactive compounds, of which three leads exhibited strong binding affinities (-7.2 to -8.2 kcal/mol) to TGFβR1 in molecular docking studies. Collectively, these findings demonstrate that GPME effectively mitigates CCl4-induced hepatic fibrosis through inhibition of TGF-β/Smad signaling, reduction of oxidative stress, and modulation of inflammatory responses, supporting its potential as a natural anti-fibrotic agent.