摘要
目的研究细胞凋亡在胃内容物吸入性肺损伤中的作用机制,并初步探讨氨溴索对肺损伤发生后细胞凋亡的影响。方法 30只健康Sprague-Dawley大鼠随机分为3组:对照组、损伤组、氨溴索组。采用蛋白免疫印迹法(Western blot)检测Bc12(B cell lymphoma/lewkmia-2)蛋白、Bax(Bc12 associated x protein)蛋白及Caspase-3蛋白表达;DNA原位末端标记(TUNEL)法测定肺组织细胞凋亡指数。结果与对照组比较,损伤组中Bax蛋白、Caspase-3蛋白表达增多,细胞凋亡指数增高;Bc12蛋白表达减少;差异均显著(P<0.05)。与损伤组比较,氨溴索组Bax蛋白、Caspase-3蛋白表达减少,细胞凋亡指数降低;Bc12蛋白表达增高;差异均显著(P<0.05)。结论细胞凋亡参与了胃内容物吸入后肺损伤发病过程,氨溴索在吸入性肺损伤组织中发挥抗细胞凋亡作用,可能机制在于调控死亡信号通路中Bax/Bc12蛋白表达相关。
Objective To study the mechanism of action of cell apoptosis in rats with gastric aspiration lung injury and to investi- gate the influence of ambroxol on cell apoptosis after lung injury. Methods 30 healthy Sprague-Dawley rats were randomly divided and e- venly into the control group, the injury group and the ambroxol group. The expressions of B cell lymphoma/lewkmia-2 （Bcl-2） , Bcl2 as- sociated x protein （Bax） and Caspase-3 were determined by Western blot, and the indexes of cell apoptosis in lung tissus were detected by TUNEL. Results The expressions of Bax and Caspase-3 were significantly higher, and the expression of Bcl-2 was obviously lower in the injury group than in the control group （ P 〈 0.05 ）. Compared with the injury group, the expressions of Bax and Caspase-3 and cell apop- totic index decreased notably in the ambroxol group （P 〈 0. 05 ） , but the expression of Bcl-2 increased obviously （P 〈 0. 05 ）. Conclusion The cell apoptosis plays an important role in the course of gastric aspiration lung injury, and ambroxol has anti-apoptotic effect on lung injury. The probable mechanism is to regulate the expression of Bax/Bcl-2 of death signaling pathway.
出处
《临床肺科杂志》
2013年第9期1572-1574,共3页
Journal of Clinical Pulmonary Medicine
关键词
氨溴索
吸入性肺损伤
细胞凋亡
ambroxol
aspiration lung injury
cell apoptosis
