OBJECTIVE AND DESIGN: The present investigation was designed to determine the effects of caffeine on alcohol-induced hepatic injury in mice. MATERIAL: Five groups of mice (8 each) were used. TREATMENT: The mice treated with different doses of caffeine (5, 10, and 20 mg/kg, respectively). METHODS: The degree of alcoholic liver injury was evaluated biochemically by measuring serum markers and pathological examination. Real time PCR and ELISA methods were used to check the expression of cytokines and CYP 450. RESULTS: Treatment with caffeine significantly attenuated the elevated serum aminotransferase enzymes and reduced the severe extent of hepatic cell damage, steatosis and the immigration of inflammatory cells. Interestingly, caffeine decreased hepatic mRNA expression of lipogenic genes, while it had no effect on protein expression of hepatic CYP2E1. Furthermore, caffeine decreased serum and tissue inflammatory cytokines levels, tissue lipid peroxidation and inhibited the necrosis of hepatocytes. Kupffer cells isolated from ethanol-fed mice produced high amounts of reactive oxygen species (ROS) and tumor necrosis factor alpha (TNF-alpha), whereas Kupffer cells from caffeine treatment mice produced less ROS and TNF-alpha. CONCLUSIONS: These findings suggest that caffeine may represent a novel, protective strategy against alcoholic liver injury by attenuating oxidative stress and inflammatory response.
OBJECTIVE AND DESIGN: The present investigation was designed to determine the effects of caffeine on alcohol-induced hepatic injury in mice. MATERIAL: Five groups of mice (8 each) were used. TREATMENT: The mice treated with different doses of caffeine (5, 10, and 20 mg/kg, respectively). METHODS: The degree of alcoholic liver injury was evaluated biochemically by measuring serum markers and pathological examination. Real time PCR and ELISA methods were used to check the expression of cytokines and CYP 450. RESULTS: Treatment with caffeine significantly attenuated the elevated serum aminotransferase enzymes and reduced the severe extent of hepatic cell damage, steatosis and the immigration of inflammatory cells. Interestingly, caffeine decreased hepatic mRNA expression of lipogenic genes, while it had no effect on protein expression of hepatic CYP2E1. Furthermore, caffeine decreased serum and tissue inflammatory cytokines levels, tissue lipid peroxidation and inhibited the necrosis of hepatocytes. Kupffer cells isolated from ethanol-fed mice produced high amounts of reactive oxygen species (ROS) and tumor necrosis factor alpha (TNF-alpha), whereas Kupffer cells from caffeine treatment mice produced less ROS and TNF-alpha. CONCLUSIONS: These findings suggest that caffeine may represent a novel, protective strategy against alcoholic liver injury by attenuating oxidative stress and inflammatory response.
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