Protective Effects And Mechanism Of Caffeine On Alcohol-induced Acute Liver Injury

Acute alcohol-induced liver injury is the substantial disposable drinking alcohol so that the volume of blood than the liver's detoxification capacity caused by acute liver injury. Pathological histology is mainly expressed in fatty degeneration of liver cell injury and inflammatory cell infiltration. Caffeine are major components of coffee and tea. At present, it is report that drinking caffeine-based beverages could reduce the prevalence of alcoholic liver disease probability, but no reports of its mechanism. Discussed on acute alcohol-induced liver injury in rats, and studyed the effects of caffeine on the body part of lesion model of cytokines, inflammatory mediators, oxygen free radicals, hepatocyte apoptosis, explored protective effect of caffeine on acute alcohol-induced liver damage. Summarized the main contents are as follows:1. Protective effects of caffeine on acute alcoholic liver injury in mice.Caffeine (5mg ? kg-1, 15mg ? kg-1, 30mg ? kg-1) can significantly reduce the elevated ALT, AST levels of serum and tissue on alcohol-induced acute liver injury mice. Caffeine (30mg ? kg-1) can decreased significantly ALT,AST contents in liver tissues. The histopathological analysis suggested that caffeine reduced the degree of hepatic steatosis in mice. 3. The mechanism of caffeine on acute alcoholic liver injury in mice.Caffeine 30mg·kg-1) can decreased significantly ALT,AST,MDA,NO contents in liver tissues. it can also significantly increase the activity GSH-PX in liver tissue. Caffeine (15mg·kg-1,30mg·kg-1) can significantly increase the activity SOD in liver tissue.Compared with model group, caffeine (5mg·kg-1,15mg·kg-1,30mg·kg-1) group can significantly reduce serum and tissue IL-1β, TNF-αlevel of experimental mice. It reveals that Caffeine have play a role protection by inhibiting tumor necrosis factor-αand IL-1βexpression in liver.α-SMA expression of model group mice is stronger than the normal group and the caffeine group (5mg·kg-1,15mg·kg-1,30mg·kg-1) mouse liver tissue. It display that caffeine can inhibit over expression ofα-SMA in the liver to protect liver.Apoptosis of liver cells of Caffeine group (15mg·kg-1,30mg·kg-1) was significantly lower than the model group. It reveals that liver cell apoptosis and giving caffeine are a negative correlation, and caffeine can inhibit cell apoptosis of the alcohol-induced liver.3. ConclusionCaffeine has a protective effect on acute alcoholic liver injury. Its mechanism may be related to anti-oxidation, inhibition of IL-1βand TNF-αlevel and inhibition of alcohol-induced liver cell apoptosis. Hepatocyte apoptosis can stimulate the hepatic stellate cell activation, it is closely related to the role of liver fibrosis, may be one of the mechanisms. It is obviously evidence that caffeine has a good anti-liver cell apoptosis, but it need to further study whether it has anti-fibrotic effect.