Paracetamol-induced hepatitis remains one of the most common models of toxic liver injury used for studying hepatoprotective agents. Excessive or prolonged intake of paracetamol leads to the formation of toxic metabolites that initiate oxidative stress, mitochondrial dysfunction, and hepatocyte necrosis. In recent years, increasing attention has been paid to natural hepatoprotectors with antioxidant and membrane-stabilizing properties, among which silymarin occupies a special place. The present study aimed to evaluate the hepatoprotective effect of silymarin in paracetamol-induced hepatitis and to analyze the main pathogenetic mechanisms underlying its protective action. The study was conducted using an experimental model of toxic liver injury induced by paracetamol administration. Biochemical markers of liver function, oxidative stress indicators, and morphological changes in hepatic tissue were assessed. The results demonstrated that paracetamol-induced hepatitis was accompanied by a significant increase in serum aminotransferases, bilirubin levels, and oxidative stress markers, indicating severe hepatocellular damage. Administration of silymarin led to a pronounced reduction in cytolytic and cholestatic syndromes, normalization of antioxidant defense parameters, and partial restoration of liver structure. These effects confirm the multifactorial hepatoprotective action of silymarin, including antioxidant, anti-inflammatory, and membrane-stabilizing mechanisms. The findings support the feasibility of using silymarin as a pathogenetically justified agent in the prevention and treatment of drug-induced liver injury.
