葶苈子对压力负荷性大鼠心室重构及神经内分泌因子和心肌I、Ⅲ型胶原的影响

目的：探讨葶苈子对压力负荷性大鼠心室重构、心肌I、Ⅲ型胶原及神经内分泌因子的影响。方法：腹主动脉不完全结扎法（abdominal aortic banding，AAB）制作大鼠心肌肥厚、心室重构模型。30d药物干预后，测量大鼠收缩压（systolic blood pressure，SBP）、舒张压（diastolic blood pressure，DBP）；称重法测定心脏指数（HW／BW、LVW／BW）；放免法测定心肌血管紧张素Ⅱ（AngⅡ）、内皮素（endothelin，ET-1），血清醛固酮（aldosterone，ALD）的水平；免疫组织化学染色法观察心肌I、Ⅲ型胶原的改变；心肌样本碱水法测定羟脯氨酸（Hydroxyproline，Hyp）的含量。结果：模型组SBP、DSP，HW／BW、LVW／BW，AngⅡ、ET-1，ALD，Hyp及I、Ⅲ型胶原含量升高（P〈0．05），免疫组化染色后观察心肌I、Ⅲ型胶原阳性表达明显增加。葶苈子水提物改善心肌肥厚指数，降低AngⅡ、ET-1，ALD及Hyp和I、Ⅲ型胶原含量作用显著（P〈0．05）。结论：葶苈子水提物通过抑制压力负荷性心室重构大鼠RAAS和交感神经系统活性，减少神经内分泌因子AngII，ET，ALD生成而抑制心肌肥大、心室重构，这可能是葶苈子直接保护心肌，抑制心肌细胞纤维化的作用机制之一。

Influnce of Tinglizi on some neuroendocrine factors and type I and III collagen in ventricular remodeling induced by abdominal aortic banding in rats]

OBJECTIVE: To approach the influnce of Tinglizi on some neuroendocrine factors and type I and III collagen in ventricular remodeling induced by Abdominal Aortic Banding (AAB) in rats. METHODS: Myocardial hypertrophy ventricular remodeling model was induced by abdominal aortic banding (AAB) in rats. After 30 day treatment, the systolic blood pressure (SBP) diastolic blood pressure (DBP) were measured; Then the ratios of LVW/BW (left ventricle weight/body weight), HW/BW (heart weight/body weight) were calculated; The Angiotensin II (Ang II) and Endothelin (ET-1) content in heart tissue and the Aldosterone (ALD) concentration of blood plasma were determined by radioimmunoassay. The content of type I and III collagen in myocardium were determined using immunohistochemical analysis. Hydroxy proline content in heart tissue was measured by hydrolysis method. RESULTS: The experimental data demonstrated that Tinglizi could decrease SBP, DBP and the cardiac indexes of LVW/BW and HW/BW, significantly reduce the content of ANg II, ALD and ET, decrease the total collagen content and type I and III collagen (P<0.05). CONCLUSION: Tiglizi can significantly attenuate the experimental ventricular remodeling; the mechanism is related with its ability to inhibit the activation of rennin-angiontensin-aldosterone system (RAAS) and systema nervosum sympatheticum (SNS), decrease the content of neuroendocrine factors (Ang II , ET, ALD).