茶多酚抗全脑缺血再灌注继发肺损伤的作用及机制研究

目的:研究茶多酚对全脑缺血再灌注引起的肺损伤的保护作用及机制。方法:采用改良的4动脉阻断法制备大鼠全脑缺血15min、再灌注3h的损伤模型。观察不同剂量茶多酚静脉内给药对大鼠脑、肺组织形态学变化、肺组织超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量以及内毒素受体CD14表达的影响。同时设立假手术组、模型组和尼莫地平组进行对照。结果:与假手术组比较,模型组大鼠脑、肺组织出现病理损伤及肺组织CD14阳性细胞的表达;与模型组比较,茶多酚与尼莫地平组均可明显升高SOD活力(P<0.05)、降低MDA含量(P<0.01)及CD14表达阳性率(P<0.01),且有明显量-效关系。结论:茶多酚可使全脑缺血再灌注大鼠脑、肺组织损伤程度明显减轻,其作用机制可能与降低肺组织内自由基含量、加强对自由基清除酶的保护作用以及减轻内毒素攻击相关。

Investigation on the Effect and Mechanisms of Tea Polyphenols on Lung Injury Caused by Global Cerebral Ischemic-reperfusion

OBJECTIVE： To investigate the protective effects of tea polyphenol （TP） on lung injury caused by global cerebral ischemic-reperfusion and its mechanism. METHODS： Improved Pulsinelli-brierley method was applied to induce damage model by global cerebral ischemia model for 15 min and global cerebral ischemia-perfusion for 3 h. Some indexes were observed, including morphology change of cerebral and lung tissue, activity of superoxide dismutase （SOD）, concentration of malondialdehyde （MDA） and expression of lipopolysaccharide receptor CD14. Healthy rats were divided into sham group, model group and nimodipine group. RESULTS： As compared with sham group, there were pathologic damage of lung and brain and the positive expression of CD14 cell of lung in model group. As compared with model group, the activity of SOD were increased significantly （P0.05） and the content of MDA and the positive expression of CD14 cell were decreased in nimodipine group （P0.01） with remarked quantity-efficacy dependent manner. CONCLUSION： TP can relieve acute lung injury caused by global cerebral ischemic-reperfusion, which is associated with reducing free radical and protecting its scavenging enzymes, relieving the attack of endotoxin.