Hepatoprotective potential of cardionogen-1, a Wnt/β-catenin signaling inhibitor against alcohol-induced chronic liver injury in C57BL/6J mice.
TL;DR
The findings of the present study suggest that CDNG-1 attenuates alcohol-induced chronic liver injury and may represent a potential therapeutic candidate for ALD.
Abstract
Alcoholic liver disease (ALD) develops following chronic alcohol consumption and is characterized by steatosis, inflammation, fibrosis, and cirrhosis. Increasing evidence suggests that dysregulated Wnt/β-catenin signaling contributes to the progression of ALD. Therefore, the present study investigated the hepatoprotective effect of cardionogen-1 (CDNG-1), a Wnt/β-catenin signaling modulator, against alcohol-induced chronic liver injury in C57BL/6 J mice. Mice were administered ethanol for 14 weeks to induce chronic liver injury, followed by treatment with CDNG-1 (50 and 100 μM/100 g, i.p.) or silymarin (100 mg/kg, p.o.) for 4 weeks. Chronic ethanol exposure elevated serum liver marker enzymes, increased oxidative stress, altered lipid metabolism-associated gene expression, and promoted inflammatory and fibrotic responses in liver tissue. CDNG-1 treatment significantly reduced serum transaminases, improved antioxidant status, and favorably regulated the expression of genes associated with alcohol metabolism, lipid dysregulation, inflammation, fibrosis, and Wnt/β-catenin signaling. Histopathological analysis also demonstrated reduced alcohol-induced hepatocellular ballooning and inflammatory infiltration following CDNG-1 treatment. The findings of the present study suggest that CDNG-1 attenuates alcohol-induced chronic liver injury and may represent a potential therapeutic candidate for ALD.