摘要
目的探讨肠淋巴液引流对失血性休克大鼠液体复苏后肺组织细胞凋亡的作用。方法18只SPF级Wistar雄性大鼠随机分成假手术组（仅麻醉与手术）、休克组（复制失血性休克模型）、休克＋引流组（复制失血性休克模型，并于休克1h后引流休克肠淋巴液）各6只，采用末端脱氧核糖转移介导的生物素化脱氧尿嘧啶缺刻标记法测定肺组织细胞凋亡，细胞核呈棕色的细胞为凋亡细胞，应用免疫组化链酶亲合素-生物素-过氧化物酶复合物法测定bcl-2和bax蛋白表达。结果休克组与休克＋引流组肺组织细胞凋亡率均显著高于假手术组，但休克＋引流组肺组织细胞凋亡率显著低于休克组。假手术组bcl-2、bax蛋白均有一定的表达；休克组肺组织细胞bcl-2表达显著低于假手术组，bax表达明显高于假手术组；休克＋引流组肺组织细胞bcl-2表达增强，bax表达降低，且休克＋引流组肺组织细胞的bcl-2表达显著高于休克组，bax表达显著低于休克组。结论肺组织细胞凋亡过度是休克后肺损伤的发生机制之一；引流休克肠淋巴液可减少肺组织细胞的凋亡，其作用机制与调节bcl-2／bax蛋白表达有关。
Objective To explore the effect of the intestinal lymph drainage on lung tissue cell apoptosis in rats with hemorrhagic shock after resuscitation, rich ALl intestinal lymphatic pathway theory. Methods TUNEL method was used to determine the apoptosis of lung tissue cells, the brown nuclei were apoptotic cells. SABC was used to determine Bcl-2 and Bax protein expression. Results The shock group and shock ＋ drainage group lung tissue cell apoptosis rate were significantly higher than those in the sham operation group, hut the shock ＋ drainage group, the apoptosis of lung tissue cells was significantly lower than the shock group. Sham operation group showed Bcl-2, Bax protein of expression ; In shock group, lung tissue cell Bcl-2 expression was significantly lower than the sham operation group, the Bax expression was significantly higher than that in the sham operation group;In shock ＋ drainage group, lung tissue cells shored enhanced expression of Bcl-2, Bax expression was reduced, and the shock ＋ drainage group lung tissue cell Bcl-2 expression was significantly higher than that in the shock group, the expression of Bax was significantly lower than the shock group. Conclusion The excessive apoptosis of lung tissue cells was one of the mechanisms of lung injury after shock. Intestinal lymph drainage could reduce lung tissue cell apoptosis, the mechanism invdved the regulation of Bcl-2/Bax protein expression.
出处
《中国基层医药》
CAS
2012年第6期801-803,I0001,共4页
Chinese Journal of Primary Medicine and Pharmacy
基金
国家自然科学基金资助项目（30370561）
河北省科学技术支撑计划（08276101D-25、11276103D-84）
