To Investigate The Role Of Blueberry Against Alcoholic Liver Injury In Rats And Mice

Objective:To investigate the effect of blueberry and its mechanism in alcoholic hepatic injury model in rats and mice.Methods:Part 1.Forty C57/6J mice were randomly divided into control group,blueberry group,blueberry+Zn PPIX group and model group.Pathological changes in the hepatic tissue by oil red O staining,the level of alanine aminotransferase(ALT),aspartate aminotransferase(AST),triglyceride(TG) and total cholesterol(TC) in serum were detected by automatic biochemical analyze.The hepatic SOD activity,GSH levels,MDA contents were quantified by ELISA.The expression of Heme Oxygenase-1(HO-1) in liver tissue was detected by Western blot.Part 2. Forty-eight healthy SD rats were randomly divided into control group, blueberry group, magnesium isoglycyrrhizinate group and model group. The rats in control group were given physiological saline, and other groups were all given 56 ml/L ethanol solution intragastrically. Blueberry group and magnesium isoglycyrrhizinate group were respective given blueberry juice and magnesium isoglycyrrhizinate solution 1 h after intragastric alcohol infusion. All SD rats were sacrificed after 4 wk. Pathological changes in the hepatic tissue by hematoxylin-eosin(HE) staining, the level of alanine aminotransferase(ALT), aspartate aminotransferase(AST), triglyceride(TG) and total cholesterol(TC) in serum were detected by automatic biochemical analyze. The activity of superoxide dismutase(SOD), the contents of tumor necrosis factor alpha(TNF-α) and the interleukin 8(IL-8) in liver homogenates were determined by enzyme linked immunosorbent assay(Elisa). The expression of toll-like receptor 4(TLR4) in liver tissue was detected by reverse transcription-PCR(RT-PCR) and Western blot.Results:Part 1. Compared with model group and blueberry+Zn PPIX group,blueberry group liver showed decreased lipid accumulation,serum ALT, AST,TG and TC levels decrease(P<0.05).The hepatic MDA also decrease(P<0.05),while GSH contents,SOD activity and the expression of HO-1 levels increase(P<0.05).While,compared with blueberry+Zn PPIX group and model group,the expression of HO-1 in blueberry group liver increase(P<0.05). Part 2. In control group, hepatocytes were found with a common radial array encircling the central veins, and no vacuoles were observed. In model group, hepatocytes were diffused with vacuoles in cytoplasm. The degrees of vacuoles in cytoplasm were significantly alleviated in blueberry group and magnesium isoglycyrrhizinate group. The level of ALT, AST, TG, TC in model group were significantly higher than blueberry group and magnesium isoglycyrrhizinate group(P<0.01). Compared to model group, the activities of SOD in liver homogenates were significantly higher(P<0.01); the contents of TNF-α, IL-8 in liver homogenates and were significantly lower(P<0.01) in blueberry group and magnesium isoglycyrrhizinate group.The expression of hepatic TLR4 in model group was significantly higher than that in blueberry group and magnesium isoglycyrrhizinate group(P<0.01). Conclusion: Blueberry possessed a protective effect on alcoholic hepatic injury in rats and mice.The mechanism might be associated with down-regulating the expression of TLR4 and the contents of hepatic TNF-α and IL-8, upregulating the activity of hepatic SOD;on the other hand,Blueberries could raise the expression of HO-1 from mice liver,increase the antioxidant capacity of liver and inhibit AFLD.