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目的:研究卡托普利对早期高血压大鼠动脉血管平滑肌细胞内质网相关因子葡萄糖调节蛋白78(glucose-regulated protein of 78 kd,GRP78)和C/EBP同源蛋白(CAAT/enhancer binding protein homologous protein,CHOP)表达的影响。方法:将18只成年雄性Sprague-Dawley(SD)大鼠随机分为对照组、模型组和卡托普利组(n=6),模型组和卡托普利组均采用大鼠腹主动脉结扎建立高血压大鼠模型。4周后测量血压,应用免疫组化方法检测主动脉血管平滑肌细胞GRP78和CHOP的表达;缺口末端标记法(TUNEL)检测细胞凋亡。结果:(1)模型组平均动脉压(mean arterial blood pressure,MAP)明显增加,卡托普利组血压低于模型组,高于对照组,差异具有统计学意义(P<0.05);(2)模型组内质网因子GRP78、CHOP表达均增加,卡托普利组GRP78、CHOP表达低于模型组,高于对照组,差异具有统计学意义(P<0.01);(3)模型组血管平滑肌细胞凋亡率减少,卡托普利组血管平滑肌细胞凋亡率高于模型组,低于对照组,差异具有统计学意义(P<0.01)。结论:卡托普利可降低高血压大鼠动脉血管平滑肌细胞GRP78和CHOP的表达,增加细胞凋亡。可能与其减弱高血压所致内质网反应,维持血管平滑肌细胞的增殖/凋亡平衡有关。
AIM: To investigate the effects of captopril on the expression of glucose-regulated protein of 78 kd (GRP78) and C / EBP homolog (CAAT) protein in arterial vascular smooth muscle cells of early hypertensive rats homologous protein (CHOP) expression. Methods: Eighteen adult male Sprague-Dawley (SD) rats were randomly divided into control group, model group and captopril group (n = 6). The model group and captopril group were treated with rat abdominal aorta Establishment of rat model of hypertension by ligation. After 4 weeks, the blood pressure was measured. The expressions of GRP78 and CHOP in aortic vascular smooth muscle cells were detected by immunohistochemistry. Apoptosis was detected by TUNEL. Results: (1) Mean arterial blood pressure (MAP) increased significantly in model group, while blood pressure in captopril group was lower than that in control group (P <0.05); (2) (P <0.01). (3) The expression of GRP78 and CHOP in the model group increased, the expression of GRP78 and CHOP in captopril group was lower than that of the model group, and the difference was statistically significant (P <0.01). (3) The apoptotic rate of smooth muscle cells was decreased, the apoptosis rate of vascular smooth muscle cells in captopril group was higher than that in model group, which was lower than that in control group (P <0.01). Conclusion: Captopril can reduce the expression of GRP78 and CHOP and increase the apoptosis of arterial smooth muscle cells in hypertensive rats. May be related to its role in attenuating the endoplasmic reticulum (ER) -induced hypertension and maintaining the proliferation / apoptosis balance of vascular smooth muscle cells.