血管活性肽对血管紧张素Ⅱ诱导高血压大鼠血管胶原重构的作用机制  

Mechanism of vasoactive peptide intermediated vascular collagen remodeling in hypertension induced by angiotensinogenⅡ

作　　者：陈光远 王秀艳 刘星群 温霞 CHEN Guangyuan;WANG Xiuyan;LIU Xingqun;WEN Xia(Department of Physical Examination,Inner Mongolia People's Hospital,Hohhot 010017,Inner Mongolia,China;Department of Emergency,Inner Mongolia People's Hospital,Hohhot 010017,Inner Mongolia,China)

机构地区：[1]内蒙古自治区人民医院体检科,内蒙古呼和浩特010017 [2]内蒙古自治区人民医院急诊科,内蒙古呼和浩特010017

出　　处：《贵州医科大学学报》2022年第8期898-903,共6页Journal of Guizhou Medical University

摘　　要：目的 探讨血管活性肽(IMD)对血管紧张素Ⅱ(AngⅡ)诱导高血压大鼠血管胶原重构的作用机制。方法 36只Sprague Dawley(SD)大鼠随机均分为AngⅡ组(肌肉注射10^(-7)mol/L AngⅡ)、AngⅡ+IMD组(肌肉注射10^(-7)mol/L AngⅡ+IMD的生理盐水)及对照组(注射同体积生理盐水),1次/d,处理2周时检测各组大鼠的尾动脉血压;60 mg/kg水和氯醛腹腔注射麻醉各组大鼠,经内眦静脉抽血,采用酶联免疫吸附剂测定(ELISA)检测各组大鼠血清Ⅰ、Ⅲ型胶原蛋白含量;取各组大鼠胸主动脉中段血管0.5 cm,苏木精-伊红染色(HE)观察血管微结构,并用ImageJ软件检测胸动脉壁厚/腔径比值(W/C)和胶原面积百分比(VFC);取各组大鼠胸主动脉血管组织200 mg,采用Western blot和实时荧光定量PCR(RT-PCR)检测大鼠血管细胞中丝裂原活化蛋白激酶(MAPK)和丝氨酸/苏氨酸激酶(Akt)的表达。结果 AngⅡ组大鼠尾动脉血压分别较对照组和AngⅡ+IMD组升高,差异均有统计学意义(P<0.05或P<0.01);与对照组相比,AngⅡ组大鼠血清中Ⅰ、Ⅲ型胶原含量、主动脉W/C及VFC升高(P<0.05),AngⅡ+IMD组大鼠血清中Ⅰ型胶原含量与主动脉W/C升高(P<0.05);与AngⅡ组相比,AngⅡ+IMD组大鼠血清中Ⅰ、Ⅲ型胶原含量及主动脉W/C及VFC升高,差异均有统计学意义(P<0.05);与对照组相比,AngⅡ组大鼠的血管细胞中p-AktmRNA表达升高(P<0.05),p-MAPKmRNA表达水平无差异(P> 0.05);与对照组相比,AngⅡ+IMD组大鼠的血管细胞中p-Aktt及p-MAPKmRNA的表达水平无变化(P> 0.05)。结论 IMD可能是通过抑制Akt及MAPK蛋白的磷酸化激活水平改善AngⅡ诱导高血压大鼠的血管胶原重构。Objective To investigate the mechanism of vasoactive peptide( IMD) in vascular collagen remodeling in angotensionogen Ⅱ ( Ang Ⅱ) induced hypertension.Methods Thirty-six Sprague Dawley(SD) rats were randomly divided into AngⅡgroup(intramuscular injection of 10^(-7)mol/L AngⅡ), AngⅡ + IMD(intramuscular injection of 10^(-7)mol/L AngⅡ + IMD normal saline),and control group(injected with equal volume of saline).All groups were treated once a day.The tail artery blood pressure was measured after two weeks.Water and chloral( 60 mg/kg) were intraperitoneally injected for anesthesia and blood was drawn from angular vein on all groups.Concentrations of collagen Ⅰ and Ⅲ in serum were tested by ELISA;HE staining was adopted to observe vascular microstructure in middle part blood vessel(0.5 cm) of thoracic aorta.ImageJ software was used to detect wall thickness/cavity diameter of thoracic aorta ratio(W/C) and collagen coverage percentage( VFC).Western blot and RT-PCR were adopted to analyze the expression of MAPK and Akt in rat vascular cells(200 mg of thoracic aorta vessel tissue).Results Caudal arterial blood pressure in Ang Ⅱ group was higher than that of control group and Ang Ⅱ + IMD group,differences were statistically significant(P< 0.05 orP< 0.01).Compared with control group, the contents of typeⅠand Ⅲ collagen, aorta W/C and VFC of Ang Ⅱ group rats increased(P< 0.05);content of typeⅠcollagen in serum and aorta W/C increased in AngⅡ + IMD group(P< 0.05).Compared with AngⅡgroup, contents of typeⅠand Ⅲ collagen, aorta W/C, and VFC of in AngⅡ +IMD group increased, and the differences were statistically significant(P< 0.05).Compared with control group, the expression ofp-AktmRNA in vascular cell of Ang Ⅱ group rats significantly increased(P< 0.05), expression ofp-MAPKmRNA showed no differences(P> 0.05).In addition,the expression ofp-AktandP-MAPKmRNA in vascular cells of Ang Ⅱ + IMD group showed no difference compared with control group(P> 0.05).Conclusion IMD may improve vascular c

关 键 词：血管紧张素Ⅱ 高血压 血管活性肽 胶原重构 磷酸化丝氨酸/苏氨酸激酶 丝裂原活化蛋白激酶 

分 类 号：R544.1[医药卫生—心血管疾病]