茶多酚干預(yù)酒精性肝病的實(shí)驗(yàn)研究.pdf

1、The activation of liver macrophages by gut-derived endotoxin and the release of　pro-inflammatory mediators have been recognized as crucial events in the development of　alcoholic liver disease (ALD). Endotoxin in complex

2、with its carrier protein, lipopolysaceharidebinding protein (LBP), is bound mainly to the CD14 receptor on Kupffer cells. This process leadsto cell activation and release of potentially cytotoxie pro-inflammatory ytokine

3、s. Tea eatechin has been shown to inhibit Cu2- induced LDL oxidation and suppresslipoxygenase activity which is a characteristic feature of ALD. It also acted as radical seavengersagainst propagating lipid peroxyl r

4、adical species. But antioxidants may not have been as effectivein humans simply owing to the kinetics of antioxidant reactions. So tea eateehin may alsoinfluence on other factors in ALD such as cytokines. We examine

5、d the expression of IL-10 in liver of ALD rat model. The immunohistochemistry analysis shows that the IL-10 expression in liver of ALD mt was elevated. When treated with teaeatechin, More IL-10 positive cells were seen,

6、with less histological damages on liver. It is ratherinteresting to see that IL-10 positive cells is mainly hepatocyte which is not a conventionalcytokine-producing cell. Then we examined the liver sample with in-sim-hyb