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目的探讨三七皂甙(Panax notoginseng saponins,PNS)对慢性血栓栓塞性肺动脉高压(Chronic thromembolismpulmonary hypertension,CTPH)大鼠心肌胶原重构的调控作用及可能的机制。方法利用二次血栓栓塞法建立大鼠CTPH模型,4周后,将正常大鼠分为A、B组,模型大鼠分为C、D组,A、C组经腹腔注射0.9%生理盐水,2 ml/d;B、D组经腹腔注射PNS,100 mg/(kg.d)。每天注射1次,4周后,测定各组大鼠的血流动力学指标、心室游离壁厚度,HE和VG染色观察心肌组织的形态学改变,Western blot检测心肌组织中基质金属蛋白酶-2(Matrix metalloproteinase-2,MMP-2)的表达。结果 C组与A组、B组比较,右心室收缩压、右室(RV)/左室(LV)游离壁厚度比、心肌间质胶原增生、MMP-2的表达均明显升高(P<0.05);经PNS干预后,D组右心室收缩压、RV/LV游离壁厚度比、心肌间质胶原增生、MMP-2的表达均明显降低(P<0.05)。结论在CTPH心肌重构过程中,PNS可以逆转右心室重构,其机制可能与上调MMP-2的表达、促进心室间质胶原的降解有关。
Objective To investigate the regulatory effect of Panax notoginseng saponins (PNS) on myocardial collagen remodeling in chronic thromboembolism pulmonary hypertension (CTPH) rats and its possible mechanism. Methods The rat model of CTPH was established by secondary thromboembolism. After 4 weeks, the normal rats were divided into A and B groups. The model rats were divided into C and D groups. The rats in A and C groups were injected intraperitoneally with 0.9% 2 ml / d. Groups B and D received intraperitoneal injection of PNS (100 mg / (kg.d)). The rats in each group were injected once a day for 4 weeks. The hemodynamic parameters, the free wall thickness of the ventricles, the morphological changes of the myocardium were observed by HE and VG staining. The expressions of matrix metalloproteinase-2 Matrix metalloproteinase-2, MMP-2). Results Compared with group A and group B, the systolic pressure of right ventricle, the ratio of free wall thickness of RV and LV, the proliferation of myocardial interstitial collagen and the expression of MMP-2 in group C were significantly increased (P < 0.05). After PNS intervention, right ventricular systolic pressure, RV / LV free wall thickness ratio, myocardial interstitial collagen hyperplasia and MMP-2 expression in group D were significantly decreased (P <0.05). Conclusion PNS can reverse right ventricular remodeling during myocardial remodeling in CTPH. The mechanism may be related to the up-regulation of MMP-2 expression and the promotion of collagen degradation.