Iranian journal of basic medical sciences · 2026
An in vivo evaluation of the antifibrotic potential of inulin against bile duct ligation-induced liver fibrosis.
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Habibian-Fard Yasaman, Ale-Ebrahim Mahsa, Mohseni-Moghaddam Parvaneh, Sarahroodi Shadi, Mortazavi Pejman
Аннотация
OBJECTIVES: Hepatic fibrosis is a major cause of liver-related mortality worldwide. This study evaluated the hepatoprotective and antifibrotic effects of inulin, a natural polysaccharide, in a rat model of cholestasis induced by bile duct ligation (BDL).
MATERIALS AND METHODS: Thirty male Wistar rats (230-250 g) were randomly divided into six groups: control, sham, inulin (200 mg/kg), BDL, and BDL+ inulin (100 and 200 mg/kg). Inulin was orally administered for 30 days after BDL. Serum liver enzyme levels, bilirubin, and lipid profiles were measured. Liver tissues were analyzed for oxidative stress markers (GPx, MDA), fibrogenic mediators (TGF-β1, α-SMA) via immunohistochemistry, and FXR levels by ELISA. Histological changes were evaluated by ELISA and Masson's trichrome staining.
RESULTS: At 200 mg/kg, inulin significantly reversed the BDL-induced increases in serum liver enzymes (AST, ALT, and ALP), total bilirubin, and cholesterol (P<0.001 vs BDL group). Hepatic GPx and FXR levels were significantly increased (P<0.001 vs BDL group), while MDA levels were decreased (P<0.001 vs BDL group). Inulin markedly suppressed the expression of TGF-β1 and α-SMA (P<0.01 vs BDL group). Histopathological evaluation showed notable improvement in liver architecture, with reduced fibrosis and necrosis (P<0.001 vs BDL group).
CONCLUSION: These findings suggest that inulin may exert antifibrotic effects through its anti-oxidant activity, ultimately reducing the expression of fibrogenic markers. This study presents strong histological evidence to support the hepatoprotective role of inulin.
MATERIALS AND METHODS: Thirty male Wistar rats (230-250 g) were randomly divided into six groups: control, sham, inulin (200 mg/kg), BDL, and BDL+ inulin (100 and 200 mg/kg). Inulin was orally administered for 30 days after BDL. Serum liver enzyme levels, bilirubin, and lipid profiles were measured. Liver tissues were analyzed for oxidative stress markers (GPx, MDA), fibrogenic mediators (TGF-β1, α-SMA) via immunohistochemistry, and FXR levels by ELISA. Histological changes were evaluated by ELISA and Masson's trichrome staining.
RESULTS: At 200 mg/kg, inulin significantly reversed the BDL-induced increases in serum liver enzymes (AST, ALT, and ALP), total bilirubin, and cholesterol (P<0.001 vs BDL group). Hepatic GPx and FXR levels were significantly increased (P<0.001 vs BDL group), while MDA levels were decreased (P<0.001 vs BDL group). Inulin markedly suppressed the expression of TGF-β1 and α-SMA (P<0.01 vs BDL group). Histopathological evaluation showed notable improvement in liver architecture, with reduced fibrosis and necrosis (P<0.001 vs BDL group).
CONCLUSION: These findings suggest that inulin may exert antifibrotic effects through its anti-oxidant activity, ultimately reducing the expression of fibrogenic markers. This study presents strong histological evidence to support the hepatoprotective role of inulin.