mTOR signaling in liver disease

The current study aimed to investigate linagliptin for its potential role in the prevention of liver fibrosis progression. Balb-C mice were randomly allocated into 5 groups (10 each), (1) control, (2) mice were injected intraperitoneally with 50 μl carbon tetrachloride (CCl4) in corn oil in a dose of 0.6 μl /g 3 times a week for 4 weeks, (3) linagliptin was orally administered in a dose of 10 mg/kg/day simultaneously with CCl4, (4) silymarin was orally in a dose of 200 mg/kg/day concomitantly with CCl4, (5) linagliptin only. Hepatic injury was manifested in CCl4 group by elevation of biochemical parameters; alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), hepatic fibrosis was evident histopathologically by increased METAVIR score and immunostaining expression of α-smooth muscle actin (α-SMA), also, increased liver tissue oxidative stress parameters, transforming growth factor-β1 (TGF-β1) and mammalian target of rapamycin (mTOR). Linagliptin was able to stop the progression of liver fibrosis; evident histopathologically with reduced METAVIR score and α-SMA expression. The possible mechanism may be via suppression of oxidative stress, TGF-β1, and mTOR, this was associated with improvement of serum biochemical parameters; ALT and AST. In conclusion, linagliptin might help to protect the liver against persistent injury-related consequences.

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mTOR signaling in liver disease

Cited by 2 publications

References 132 publications

Endocytosis in Liver Function and Pathology

Endocytosis in Liver Function and Pathology

Hepatoprotective effect of linagliptin against liver fibrosis induced by carbon tetrachloride in mice

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