Experimental Study Of Chaizhi Mistura In Treatment Of Chronic Alcoholic Liver Injury

AIM To evaluate the therapeutic effects of Chaizhi mistura on chronic alcoholic liver injury in rats and to study the possible action mechanism of this prescription to protect against the liver injury. METHODS A animal model of chronic alcoholic liver injury was established by oral 60% alcoholic solution to rats for 24 weeks. The rats were treated with Chaizhi mistura for 2 weeks, and simultaneously a comparison is made between Chaizhi mistura and Dongbaogantai. The following indexes is determined and observed: (l)the activity of Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST), Alkaline Phosphatase (ALP), Gamma-Glutamyl Transferase (GGT) in serum; (2) the level of total Cholesterol (Chol), Triglycerido (TG) in serum; (3) the activity of erythrocyte superoxide dismutase (SOD), DT-Diaphorase (DTD), Glutathion peroxidase (GSH-Px) and the content of lipid peroxides (LPO) of hepatic microsomal supernatant fluid ; ( 4 ) the content of lipid-soldeflorescent pigment (L5FP) of hepatic mitochondria; (5) the content of total membrane phospholipid (PL), total Cholesterol (Chol), pho sphatidylcholines (PC), phosphatidylethanolanine (PE), phosphatidyl serine (PS), phosphatidylinositol (P1), sphingomyelin (SM) of hepatic membrane; (6) the change of hepatic pathology RESULTS A animal model of chronic alcoholic liver injury could be established by oral 60% alcoholic solution to rats for 24 weeks, then stabilized in 2 weeks. Contrast to natural recovery group, Chaizbi mistura could promote the recovery of fatty degeneration in liver organization, reduce the activity of ALT, AST, ALP, GGT in serum; elevate the level of Chol and reduce the level of TG in serum; elevate the activity of SOD, DTD of hepatic microsomal supernatant fluid; reduce the content of LPO of hepatic microsomal supernatant fluid and LsFP of hepatic mitochondria; reduce the content of Chol, SM and elevate PC, PE of hepatic membrane; decrease aging index of membrane of C/P, SM/PC. CONCLUSION The action mechanisms are as follows: 1 Antagonist fatty degeneration of the alcoholic liver injury; 2 Promote the recovery of liver cell function; 3 Regulate lipid metabolism; 4 Anti-lipidperoxidation; 5 Protect hepatic cell membrane, protect against membrane aging.