茶多酚对肺缺血再灌注损伤大鼠的保护作用

目的：研究茶多酚对肺缺血再灌注损伤大鼠的保护作用。方法将100只大鼠按随机数字表法分为假手术组，模型组，茶多酚低、中、高剂量组各20只。茶多酚低、中、高剂量组分别尾静脉注射茶多酚溶液25、50、100 mg/kg，假手术组和模型组分别给予等体积生理盐水。除假手术组外，其余各组大鼠于给药后30 min，采用夹闭左肺门后松夹的方法制备肺缺血再灌注损伤大鼠模型。缺血45 min再灌注120 min后，测定各组大鼠PO2、肺组织湿/干重比；通过原位细胞凋亡检测法观察肺组织细胞凋亡并计算凋亡指数；测定肺组织中SOD、MDA、过氧化氢酶水平。结果与模型组比较，茶多酚中、高剂量组大鼠肺组织湿/干重比[(5.7±0.4)、(5.5±0.4)比(6.5±0.5)]、凋亡指数[(19.3±1.8)%、(14.2±1.4)%比(31.2±2.4)%]降低(P＜0.05或P＜0.01)，肺组织中SOD[(115.2±18.1)U/mg、(128.7±20.9)U/mg比(94.7±12.1)U/mg]、过氧化氢酶[(1.3±0.2)U/mg、(1.7±0.4)U/mg 比(0.9±0.2)U/mg]水平升高， MDA[(1.1±0.3)nmol/L、(1.0±0.3)nmol/L比(1.6±0.5)nmol/L]水平降低(P＜0.05或P＜0.01)；茶多酚高剂量组 PO2[(93.4±4.0)%比(85.9±3.4)%]较模型组升高(P＜0.01)。结论茶多酚可提高肺缺血再灌注损伤大鼠动脉血氧分压、降低肺组织湿/干重比、抑制肺组织细胞凋亡，对肺缺血再灌注损伤大鼠具有保护作用。

Protection of tea polyphenols against pulmonary ischemia-reperfusion injury in rats

Objective To investigate the protection of tea polyphenols (TP) against pulmonary ischemia-reperfusion injury in rats. Methods A total of 100 rats were randomly devided into five groups:the sham operation group, the model control group, the high-, medium-and low-dose TP groups. Two hours after reperfusion, the PO2 and the lung tissue wet/dry (W/D) ratio were examined; the apoptosis index (AI) was analysised;the activity of SOD, CAT and the content of MDA in lung tissue were determined. Results Compared with the model control group, the W/D (5.7 ± 0.4, 5.5 ± 0.4 vs. 6.5 ± 0.5) and the AI (19.3%± 1.8%, 14.2%± 1.4%vs. 31.2%± 2.4%) of the high-, medium-dose groups were significantly decreased (P<0.05 or P<0.01);the activity of SOD (115.2 ± 18.1 U/mg, 128.7 ± 20.9 U/mg vs. 94.7 ± 12.1 U/mg), CAT (1.3 ± 0.2 U/mg, 1.7 ± 0.4 U/mg vs. 0.9 ± 0.2 U/mg) in lung tissue of the the high-, medium-dose groups groups were significantly increased (P<0.05 or P<0.01), and the content of MDA (1.1 ± 0.3 nmol/L, 1.0 ± 0.3 nmol/L vs. 1.6 ± 0.5 nmol/L) were significantly decreased (P<0.05 or P<0.01). The PO2 (93.4%± 4.0%vs. 85.9%± 3.4%) of the high-dose group were significantly increased compared to the model group (P<0.01). Conclusion TPs could effectively lower the W/D, increase the PO2, inhibit the hepatocyte apoptosis, lower the AI, suggesting that TPs had protective effects against pulmonary ischemia-reperfusion injury in rats, which perhaps related to its effects of improving antioxidant ability and inhibiting the oxidative stress.