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目的 :探讨血管紧张素Ⅱ (AngⅡ )受体拮抗剂氯沙坦对血管损伤性重塑的作用及其内在机制。 方法 :将Wistar大鼠随机分为假手术组 (6只 )、氯沙坦组 (2 0只 )及对照组 (2 1只 ) ,后两组大鼠行胸主动脉球囊损伤术 ,术后不同时间段处死。三组均进行苏木精 伊红染色及计算机图像分析 ,Tunel标记法检测细胞凋亡率 ,免疫组化方法检测血管壁凋亡相关基因表达物Fas、Fas L、Bcl 2、Bax的变化。结果 :对照组术后第 7、14天损伤血管管壁横截面积增加明显 ,分别为 (0 .4 84± 0 .180 )mm2 和 (0 .6 6 1± 0 .2 4 1)mm2 ,与假手术组比较 ,P <0 .0 5。术后第 14天 ,氯沙坦组损伤血管管壁横截面积为 (0 .384± 0 .0 90 )mm2 ,与对照组比较 ,管壁增生程度显著降低。术后第 7天 ,管壁面积增生比与细胞凋亡率之间有负相关性 (r =- 0 .5 86 ,P <0 .0 5 ) ,氯沙坦组的细胞凋亡率显著高于对照组。氯沙坦组与对照组比较 ,术后第 7天管壁组织内Fas L表达增加 ,Bcl 2表达降低 (P <0 .0 5 )。结论 :AngⅡ受体拮抗剂氯沙坦可有效减轻大鼠动脉损伤后的血管增生性重塑。其机制可以与促进细胞Fas的表达、抑制Bcl 2的表达 ,从而增加细胞凋亡率有关
Objective: To investigate the role of losartan, an angiotensin Ⅱ receptor antagonist, in vascular remodeling and its underlying mechanism. Methods: Wistar rats were randomly divided into sham operation group (6), Losartan group (20) and control group (21). The latter two groups were performed thoracic aortic balloon injury After different periods of execution. Hematoxylin and eosin staining and computer image analysis were performed in all three groups. The apoptosis rate was detected by Tunel labeling method. The expressions of Fas, Fas L, Bcl 2 and Bax were detected by immunohistochemistry. Results: At the 7th and 14th day after operation, the cross-sectional area of vascular wall in the control group increased significantly ((0.84 ± 0.80) mm2 and (0.666 ± 0.241) mm2, Compared with the sham operation group, P <0.05. On the 14th postoperative day, the cross-sectional area of vascular wall in losartan group was (0.384 ± 0.903) mm2, which was significantly lower than that in control group. On the 7th day after operation, there was a negative correlation between the rate of cell wall hyperplasia and cell apoptosis rate (r = - 0.586, P <0.05), and the apoptosis rate of losartan group was significantly higher In the control group. Losartan group compared with the control group, 7 days after the tube wall tissue Fas L expression increased, Bcl 2 expression decreased (P lt; 0.05). CONCLUSION: Losartan, an antagonist of angiotensin Ⅱ, can effectively attenuate angiogenic remodeling after arterial injury in rats. The mechanism may be related to promoting the expression of Fas, inhibiting the expression of Bcl 2 and increasing the rate of apoptosis