Assessment of Hepato-Protective Potential of a Sinapic Acid on Animal Model of Alcohol Induced Hepatotoxicity

Background:
Alcoholic liver disease (ALD) remains one of the major causes of liver-related morbidity and mortality worldwide. Oxidative stress and inflammation are key mechanisms driving hepatic injury. Sinapic acid (SA), a naturally occurring phenolic compound abundant in cereals, oilseeds, and vegetables, is recognized for its antioxidant and anti-inflammatory properties and has been identified in several traditional medicinal formulations.

Methods:
The present study evaluated the hepatoprotective efficacy of SA in Wistar albino rats exposed to ethanol-induced hepatotoxicity. Liver injury was induced by oral administration of ethanol (40%) for 21 days. SA was administered at doses of 40, 80, and 100 mg/kg p.o., and its protective effects were assessed through biochemical markers (SGOT, SGPT, ALP, total cholesterol, triglycerides, HDL), antioxidant parameters (GSH, MDA, CAT, SOD), proinflammatory cytokines (TNF-α, IL-6), and histopathological examination.

Results:
Ethanol exposure markedly increased ALT (154.2 ± 6.3 IU/L), AST (178.5 ± 8.1 IU/L), and ALP (326.4 ± 10.2 IU/L) compared with normal controls (48.3 ± 3.1, 72.6 ± 4.8, and 162.7 ± 7.5 IU/L; p < 0.001). SA at 80 and 100 mg/kg significantly reduced these levels, with ALT at 82.4 ± 5.2 and 76.8 ± 4.9 IU/L and AST at 102.3 ± 6.1 and 96.7 ± 5.4 IU/L. GSH levels increased from 18.3 ± 1.2 to 32.5 ± 1.8 µmol/mg, while MDA decreased from 7.4 ± 0.5 to 3.2 ± 0.3 nmol/mg (p < 0.001). qRT-PCR revealed downregulation of TNF-α and IL-6 by 68% and 61%, respectively. Histological findings confirmed reduced necrosis and inflammation with near-normal hepatic architecture in treated groups.

Conclusion:
Sinapic acid exhibits strong hepatoprotective effects against alcohol-induced liver injury, likely through attenuation of oxidative stress and inflammatory pathways. These findings support its potential as a natural therapeutic candidate for managing ALD.