<p>The present study evaluated the in-vivo antioxidant and hepatoprotective potential of the methanolic extract of <i>Sterculia villosa Roxb.</i> bark in an Acetaminophen (APAP)-induced acute liver injury model in Wistar albino rats, supported by molecular docking analysis. Animals were randomly allocated into five groups and treated orally for 7 days: Group I (normal control) received 0.9% saline; Group II (toxic control) received APAP (2&#xa0;g/kg); Group III (reference control) received APAP (2&#xa0;g/kg) plus Silymarin (50&#xa0;mg/kg); Group IV received APAP (2&#xa0;g/kg) plus extract (200&#xa0;mg/kg); and Group V received APAP (2&#xa0;g/kg) plus extract (400&#xa0;mg/kg). Hepatic injury was induced by administering APAP three hours before the final treatment on day 7, followed by sacrifice and sample collection after 48&#xa0;h. Serum biochemical markers ALT, AST, and ALP, along with lipid profile parameters (total cholesterol, triglycerides, High-density lipoprotein, Low-density lipoprotein, and non-HDL cholesterol) were assessed. Antioxidant defense markers including, GPx, SOD, and CAT were measured in liver homogenates, and histopathology was performed to confirm tissue-level changes. APAP administration significantly increased liver enzyme levels and disrupted lipid homeostasis while significantly reducing hepatic antioxidant enzyme activities. Methanolic extract of <i>S. villosa</i> bark treatment, particularly at 400&#xa0;mg/kg, significantly reduced ALT, AST, and ALP and improved lipid abnormalities compared with the toxic control, with partial recovery of GPx, SOD, and CAT activities. Histopathological findings supported these biochemical outcomes by showing improved hepatic cytoarchitecture in extract-treated groups. In silico molecular docking further suggested that several <i>S. villosa</i> phytocompounds exhibit notable binding affinity toward ALT, AST, and ALP, indicating potential enzyme-interaction mechanisms. Overall, the methanolic extract of <i>S. villosa</i> bark demonstrated dose-dependent hepatoprotective and antioxidant effects against APAP-induced liver injury, not statistically different from Silymarin at the higher dose.</p>

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Preclinical Investigation of Hepatoprotective Effects of Sterculia villosa Roxb. in Acetaminophen-Induced Liver Injury: In Vivo and Molecular Docking Approaches

  • Chadni Lyzu,
  • Samina Akhter,
  • Dipankar Chandra Roy,
  • Talha Bin Emran,
  • Samina Yesmin,
  • Mohammed A. Satter,
  • Dipa Islam,
  • Evena Parvin Lipy,
  • Md. Nazim Uddin

摘要

The present study evaluated the in-vivo antioxidant and hepatoprotective potential of the methanolic extract of Sterculia villosa Roxb. bark in an Acetaminophen (APAP)-induced acute liver injury model in Wistar albino rats, supported by molecular docking analysis. Animals were randomly allocated into five groups and treated orally for 7 days: Group I (normal control) received 0.9% saline; Group II (toxic control) received APAP (2 g/kg); Group III (reference control) received APAP (2 g/kg) plus Silymarin (50 mg/kg); Group IV received APAP (2 g/kg) plus extract (200 mg/kg); and Group V received APAP (2 g/kg) plus extract (400 mg/kg). Hepatic injury was induced by administering APAP three hours before the final treatment on day 7, followed by sacrifice and sample collection after 48 h. Serum biochemical markers ALT, AST, and ALP, along with lipid profile parameters (total cholesterol, triglycerides, High-density lipoprotein, Low-density lipoprotein, and non-HDL cholesterol) were assessed. Antioxidant defense markers including, GPx, SOD, and CAT were measured in liver homogenates, and histopathology was performed to confirm tissue-level changes. APAP administration significantly increased liver enzyme levels and disrupted lipid homeostasis while significantly reducing hepatic antioxidant enzyme activities. Methanolic extract of S. villosa bark treatment, particularly at 400 mg/kg, significantly reduced ALT, AST, and ALP and improved lipid abnormalities compared with the toxic control, with partial recovery of GPx, SOD, and CAT activities. Histopathological findings supported these biochemical outcomes by showing improved hepatic cytoarchitecture in extract-treated groups. In silico molecular docking further suggested that several S. villosa phytocompounds exhibit notable binding affinity toward ALT, AST, and ALP, indicating potential enzyme-interaction mechanisms. Overall, the methanolic extract of S. villosa bark demonstrated dose-dependent hepatoprotective and antioxidant effects against APAP-induced liver injury, not statistically different from Silymarin at the higher dose.