活血潜阳颗粒逆转自发性高血压大鼠左心室肥厚的实验研究

目的探讨活血潜阳颗粒逆转高血压左心室肥厚的作用机制。方法以自发性高血压大鼠(sponta-neoushypertensionrats,SHR)为高血压及高血压左心室肥厚模型,随机分为活血潜阳颗粒高、中、低剂量治疗组,卡托普利治疗组,松龄血脉康治疗组和模型组,并以正常血压Wistar-Kyoto大鼠为正常对照组,检测大鼠尾动脉收缩压(systolicbloodpressure,SBP)及左心室质量指数(leftventricularmassindex,LVMI),放免法测定大鼠左心室组织血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)含量,应用免疫组化法、RT-PCR法观察左心室组织血管紧张素转换酶(angiotensinconvertingenzyme,ACE)蛋白与mRNA表达。结果(1)与正常对照组比较,模型组SBP、LVMI值显著升高;与模型组比较,活血潜阳颗粒高、中剂量可显著降低SBP、LVMI值,其作用与松龄血脉康治疗组比较,差异无统计学意义,但作用明显差于卡托普利治疗组;(2)与正常对照组比较,模型组左心室组织AngⅡ含量升高,ACE蛋白、mRNA表达明显上调;与模型组相比,活血潜阳颗粒高、中、低剂量可减少心脏局部AngⅡ的含量,下调SHR左室心肌ACE蛋白及mRNA表达,其下调作用与松龄血脉康治疗组比较,差异无统计学意义,但其作用明显不及卡托普利治疗组。结论活血潜阳颗粒可逆转SHR左心室肥厚,其作用机制可能与下调左室心肌ACE蛋白及mRNA的表达,减少心脏局部AngⅡ的含量有关。

Study of Huoxue Qianyang Granules in revising the left ventricular hypertrophy of spontaneous hypertension rats

OBJECTIVE: To study the mechanism of Huoxue Qianyang Granule (HXQYG), a traditional Chinese compound medicine, in revising the left ventricular hypertrophy of hypertension. METHODS: Spontaneous hypertension rats (SHR) were randomly divided into seven groups: untreated group, Songling Xuemaikang (SLXMK)-treated group, captopril-treated group, high-, medium- and low-dose HXQYG-treated groups, and normal control group. The systolic blood pressure (SBP) and left ventricular mass index (LVMI) were measured. The content of angiotensin II (Ang II) in left ventricular tissue was determined by radioimmunoassay. The expressions of angiotensin converting enzyme (ACE) protein and mRNA in left ventricular tissue were analyzed separately by immunohistochemical method and RT-PCR. RESULTS: (1) SBP and LVMI were higher in the untreated group than those in the normal control group, and they were lower in the high- and medium-dose HXQYG-treated groups than those in the untreated group, but higher than those in the captopril-treated group, and without significant difference as compared to those in the SLXMK-treated group. (2) The content of Ang II and expressions of ACE protein and mRNA in the left ventricular tissue in the untreated group were higher than those in the normal control group, and they were lower in the HXQYG-treated groups than those in the untreated group, but higher than those in the captopril-treated group, and without significant difference as compared to those in the SLXMK-treated group. CONCLUSION: HXQYG can reverse the left ventricular hypertrophy of SHR, which may be due to decreasing the amount of Ang II and expressions of ACE protein and mRNA in the left ventricular tissue.