依达拉奉对急性肺损伤大鼠肺组织凋亡的影响

发布时间：2018-04-29 15:07

本文选题：急性肺损伤 + 依达拉奉　；参考：《中国老年学杂志》2017年18期

【摘要】：目的探讨依达拉奉治疗急性肺损伤(ALI)大鼠的作用及其机制。方法将48只清洁级Wistar成年大鼠随机分为对照组、ALI组和依达拉奉(EDA)组,之后给予EDA治疗。治疗后第7天留取肺脏组织,行苏木素-伊红(HE)染色观察肺组织形态,Western印迹和免疫组织化学法检测肺组织Bcl-2和Bax表达。结果 HE染色显示ALI组肺组织表现肺结构部分破坏,肺泡部分肺泡壁塌陷且水肿严重,部分肺泡腔扩大,大量炎性细胞浸润,肺泡隔显著增厚,明显的局部出血;与ALI组相比,EDA组肺组织结构破坏较轻,水肿也明显减轻,仅有少量炎性细胞浸润。Western印迹结果显示,与ALI组相比,EDA组抗凋亡蛋白Bcl-2的表达水平明显增高,促凋亡蛋白Bax表达水平显著降低,酶切-caspase3蛋白表达明显下调(均P0.01)。免疫组化结果表明,与ALI组相比,核浆中的Bcl-2表达水平明显增高,Bax表达水平明显降低(均P0.01)。结论 EDA在ALI大鼠肺组织中上调Bcl-2和下调Bax蛋白水平来降低细胞凋亡,同时其可能通过减少Caspase3依赖途径的凋亡来保护肺组织。
[Abstract]:Objective to investigate the effect and mechanism of Edaravone on acute lung injury (Ali) rats. Methods Forty-eight clean grade Wistar adult rats were randomly divided into two groups: control group and Edaravone group. Then they were treated with EDA. Lung tissues were collected on the 7th day after treatment. The expression of Bcl-2 and Bax in lung tissues were detected by Western blot and immunohistochemistry. The lung tissues were stained with hematoxylin and eosin (HEH). Results HE staining showed partial destruction of lung structure, collapse and edema of alveolar wall, enlargement of alveolar cavity, infiltration of inflammatory cells, thickening of alveolar septum and obvious local hemorrhage in ALI group. Compared with ALI group, the lung tissue structure was slightly damaged and edema was alleviated. Only a small amount of inflammatory cells infiltrated. Western blot results showed that the expression of anti-apoptotic protein Bcl-2 was significantly higher in EDA group than in ALI group. The expression of pro-apoptotic protein Bax was significantly decreased, and the expression of enzyme digested caspase3 was significantly down-regulated (P 0.01). The results of immunohistochemistry showed that the expression of Bcl-2 in nuclear plasma was significantly higher than that in ALI group (P 0.01). Conclusion EDA can decrease apoptosis by up-regulating Bcl-2 and down-regulating the level of Bax protein in the lung tissue of ALI rats, and it may protect lung tissue by reducing the apoptosis of Caspase3 dependent pathway.
【作者单位】：香港大学深圳医院;吉林大学第一医院;吉林大学基础医学院;吉林大学中日联谊医院;
【基金】：基金项目:吉林省卫生计生委(2015SZC13)
【分类号】：R563.8

【相似文献】