CAJ | 학술논문

目的：本研究目的是利用厄贝沙坦、血管紧张素Ⅱ（AngⅡ）干预平滑肌细胞，阐明血管紧张素Ⅱ受体阻滞剂（ARB）对血管紧张素Ⅱ1型受体（AT1R）表达及其下游信号通路的影响。方法利用Western Blot技术，研究厄贝沙坦、血管紧张素Ⅱ干预平滑肌细胞后对细胞AT1受体蛋白表达及其下游信号通路-细胞外信号调节激酶1/2（ERK1/2）和信号转导子和转录激活子3（STAT3）蛋白磷酸化水平的影响。结果研究发现厄贝沙坦能显著地抑制AngⅡ诱导的AT1受体蛋白表达（0.208±0.022 vs 0.997±0.131，P<0.01）及下游信号通路中的ERK1/2蛋白磷酸化（0.055±0.007 vs 0.103±0.020，P<0.01）、STAT3蛋白磷酸化（0.162±0.010 vs 0.758±0.054，P<0.01）。结论这些研究结果表明厄贝沙坦抑制AT1R和下游的ERK1/2及STAT3信号通路，从而抑制AngⅡ诱导的平滑肌细胞增殖等，发挥控制血压、防治心脑血管疾病作用。
목적：본연구목적시이용액패사탄、혈관긴장소Ⅱ（AngⅡ）간예평활기세포，천명혈관긴장소Ⅱ수체조체제（ARB）대혈관긴장소Ⅱ1형수체（AT1R）표체급기하유신호통로적영향。방법이용Western Blot기술，연구액패사탄、혈관긴장소Ⅱ간예평활기세포후대세포AT1수체단백표체급기하유신호통로-세포외신호조절격매1/2（ERK1/2）화신호전도자화전록격활자3（STAT3）단백린산화수평적영향。결과연구발현액패사탄능현저지억제AngⅡ유도적AT1수체단백표체（0.208±0.022 vs 0.997±0.131，P<0.01）급하유신호통로중적ERK1/2단백린산화（0.055±0.007 vs 0.103±0.020，P<0.01）、STAT3단백린산화（0.162±0.010 vs 0.758±0.054，P<0.01）。결론저사연구결과표명액패사탄억제AT1R화하유적ERK1/2급STAT3신호통로，종이억제AngⅡ유도적평활기세포증식등，발휘공제혈압、방치심뇌혈관질병작용。
ObjectiveTo explore the effects of the angiotensintype1-receptor blockers (ARB) on the expression of angiotnsinⅡ type 1 receptor. MethodsIrbesartan was added into cultured vascular smooth muscle cells (VSMCs). AngiotensinⅡ type 1 (AT1) recetpor protein expression were detected with western blot, at the same time, the signalling pathway of (extracellular signal-regulated kinase 1/2)ERK1/2 and (Signal Transducer and Activator of Transcription 3) STAT3 AT1 receptor actived were also detected.ResultsIt was found that Irbesartan inhibit signiifcantly AT1 receptor protein expression, not only in the absence , but also in the presence of AngⅡ. Similar to AT1 receptor protein expression, the signal ERK1/2 and STAT3 phosphorylation was obviously inhibited while Irbesartan intervention.ConclusionThis study data show that Irbesartan was able to inhibit AT1 receptor expression and signal pathway of ERK1/2 and STAT3 phosphorylation.