表没食子儿茶素没食子酸酯对小鼠油酸型肺损伤的保护作用

目的研究表没食子儿茶素没食子酸酯(EGCG)对油酸型小鼠肺损伤的保护作用，并探讨其作用机制。方法以油酸型小鼠为研究对象，利用光镜、电镜观察肺部形态学变化，称重法计算肺指数及湿/干重比(w/d)，应用酶联免疫吸附法(ELISA)检测血清中TNF-α含量及Western blotting法测定肺组织中p38 MAPK的磷酸化程度。结果EGCG可明显减轻油酸组小鼠肺组织病理学改变，降低肺指数及肺湿/干重比，降低血清中炎症因子TNF-α的含量，抑制肺组织中p38 MAPK的磷酸化。结论EGCG有明显的抗油酸型小鼠肺损伤的作用，其作用机制可能与抑制p38 MAPK的磷酸化，并最终导致TNF-α的合成与释放减少有关。

Effect of epigallocatechingallate on acute lung injury induced by oleic acid in mice

AIM: To investigate the effect of epigallocatechingallate (EGCG) on acute lung injury induced by oleic acid in mice and the possible mechanism. METHODS: Acute lung injury was induced by oleic acid in mice. Light microscopy and electron microscopy were used to examine histological changes and lung index as well as wet to dry weight ratio was calculated. Serum TNF-a level was measured by enzyme linked immunosorbent assay (ELISA) and the phosphorylation of p38 MAPK was determined by Western blotting. RESULTS: Pretreatment of EGCG significantly alleviated oleic acid induced lung injury accompanied by reduction of lung index and wet to dry weight ratio, decreased of TNF-a level in serum and inhibition of phosphorylation of p38 MAPK. CONCLUSION: EGCG showed beneficial effect on acute lung injury induced by oleic acid in mice. The ultimate reduction of TNF-alpha in serum caused by inhibition of phosphorylated p38 MAPK is involved in the mechanism of action of EGCG.