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胰激肽原酶对自发性高血压大鼠心肌转化生长因子-β_1表达及一氧化氮含量的影响

Effect of pancreatic kininogenase on expression of TGF-β1 and nitrol oxide level in spontaneously hypertensive rats
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摘要 目的观察胰激肽原酶对自发性高血压大鼠(SHR)左室肌转化生长因子-β1(TGF-β1)表达及血清一氧化氮(NO)含量的影响,探讨其降压和逆转左室重构的药理机制。方法雄性15周龄SHR 24只,随机分成SHR组、胰激肽原酶组、卡托普利组,每组8只,另取8只雄性同龄健康W istar大鼠(WKY)作为正常血压对照组。4 w后行颈动脉插管测量血压,抽血测血清NO含量,处死动物,取出心脏行左室重量指数测定,心肌组织经VG染色作形态学观察及胶原测定,用免疫组化SP法检测心肌组织切片内TGF-β1的表达。结果SHR组收缩压(SBP)、左心室重量指数(LV-M I)、心肌胶原体积比例(CVF)和心肌血管周围胶原与管腔面积的比例(PVCA)及TGF-β1的表达较WKY组明显升高,NO含量明显下降(P<0.05),应用胰激肽原酶后,NO含量明显上升,余各指标均显著性下降(P<0.05)。除SBP外,胰激肽原酶组各指标变化程度均与卡托普利组无差异。结论胰激肽原酶具有降低血压和逆转心室重构的作用,其机制可能与增加NO含量及抑制心室肌高表达的TGF-β1有关。 Objective To investigate the effect of pancreatic kininogenase on the expression of TGF-β1 and nitrol oxide (NO) level in myocardium of spontaneously hypertensive rats (SHRs) and to explore its pharmacological mechanism for reducing blood pressure and reversing left ventricular remodeling. Methods 24 maJe fifteen-week SHRs were randomly divided into SHR group, pancreatic kininogenase group,captoprill group (n =8 in each) ,8 male fifteen-week Wistar Kyoto (WKY) was selected as control group. After four weeks, blood pressure of all the rats were measured through carotid artery, intubation to detect serum NO level. Then the rats were sacrificed to determine left ventricular mass index (LVMI) and stain myocardial tissue with VE and to detect collagen volume fraction (CVF). TGF-β1 expressions were detected by immunohistochemical technique (SP method). Resells In SHRs group, systolic blood pressure. (SBP), LVMI, CVF, perivascular circumferential area (PVCA) and expression of TGF-β1 were higher, serum NO level was decreased obviously than those in WKY group (P〈 0.05). After using pancreatic kininogenase therapy, serum NO level was raised, and closed to normal level, all other indexes were decreased obviously than those in SHR group ( P 〈 0.05 ). There was no difference between pancreatic kininogenase group and captoprill group except SBP. Conclusions Pancreatic kininogenase could obviously increase NO level and suppress the expression of TGF- βin myocardial tissue, by which reduces ventricular remodeling in SHRs.
出处 《中国老年学杂志》 CAS CSCD 北大核心 2006年第10期1366-1368,共3页 Chinese Journal of Gerontology
关键词 胰激肽原酶 转化生长因子-Β1 一氧化氮 心室重构 Pancreatic kininogenase TGF-β1 Nitrol oxide Ventricular remodeling
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