ABSTRACT
Objective To study the influence of total flavonoids of hemerocallis fulva(TFHF) on hepatocyte apoptosis and related protein expression in mice with alcoholic hepatic injury.Methods A total of 40 mice were randomly divided into four groups:blank control,model control andsmall and high dose TFHF groups,10 cases in each group.The mice were given the continuous gavage administration for 7 d.Then the model group was given once gavage by 50％ ethanol 12.0 mL/kg after 1 h of the last administration.The blank control group was given the equal volume of distilled water.The activity levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum as well as the superoxide dismutase(SOD) activity and malondialdehyde (MDA) content in liver tissue hemogenate were detected.Hematoxylin and Eosin(HE) staining was performed for observing the pathological changes of the liver tissue.The flow cytometer was used to test the apoptosis ratio in hepatocyte suspension.The expressions of caspase-3,Bcl-2 and Bax protein were detected by Western blot.Results The various TFHF groups could decrease the activities of ALT and AST in serum (P＜0.05),while could decrease the MDA content in liver tissue hemogenate (P＜0.01) and increased the SOD activity;the liver tissue pathological examination showed that the high dose TFHF group could make the liver cell degeneration,alleviated the necrosis degree and relieved the pathological change of hepatic tissue;compared with the model group,the hepatocyte apoptosis rate in each TFHF group was decreased significantly;Western blotting results showed that the caspase-3 protein level in each TFHF group was decreased,expression of Bcl-2 protein was increased,whereas which of Bax protein was decreased and Bax/Bcl-2 ratio was reduced.Conclnsion TFHF has obvious protective effect on mice acute hepatic injury induced by ethanol,and can inhibit the hepatocyte apptosis,its action mechanism may be related to its antioxidation and regulation of caspase-3,Bcl-2 and Bax expression.
ABSTRACT
OBJECTIVE:To explore the protective effect and its mechanisms of Sinomenium acutum polysaccharide on mice with acute alcoholic liver injury. METHODS:60 mice were randomly divided into blank control group (normal saline),model group (normal saline),bifendate group (positive control,150 mg/kg) and S. acutum polysaccharide low-dose,medium-dose, high-dose groups(100,200,400 mg/kg),10 in each group,intragastrically administrated,once a day,for continual 7 d. 1 h af-ter last administration,mice received 50% ethanol (0.1 mL/10 g) intragastrically to induce acute alcoholic liver injury model ex-cept for those in blank control group. After 12 h,alanine aminotransferase(ALT),aspartate aminotransferase(AST)levels in se-rum,malondialdehyde(MDA),superoxide dismutase(SOD),glutathione(GSH),glutathione peroxidase(GSH-Px)levels in liv-er tissue of mice were determined;hematoxylin-eosin staining was conducted to observe the pathological changes in liver tissue;flow cytometry was used to detect the cell apoptosis rate. RESULTS:Compared with blank control group,mice in model group showed pathological changes in edema,disordered cell arrangement and local necrosis;ALT and AST levels in serum,MDA level in liver tissue and hepatocyte apoptotic rate were significantly increased,while the SOD,GSH and GSH-Px levels in liver tissue were significantly decreased,with statistical significances (P<0.01). Compared with model group,cell degeneration and necrosis degree of mice were improved in S. acutum polysaccharide medium-dose and high-dose groups;except for cell apoptosis rate of liver in S. acutum polysaccharide low-dose group was not decreased significantly,the above-mentioned indicators in other treatment groups were significantly improved(P<0.05 or P<0.01). CONCLUSIONS:S. acutum polysaccharide shows obvious protective effect on mice with acute alcoholic liver injury,its mechanism might re-late to anti-oxidation stress and inhibiting hepatocyte apoptosis.
