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目的观察芩丹胶囊对老年自发性高血压(SHR)大鼠血管壁Ⅰ型胶原蛋白和基因表达的影响,并进一步探讨其对血管重构的作用机制。方法 32只40周龄老年自发性高血压大鼠模型随机分为模型组(SHR组)、芩丹胶囊大剂量组(SHR+QDH组)、芩丹胶囊小剂量组(SHR+QDL组)、氯沙坦组(SHR+Los组),另设老年Wistar-Kyoto(WKY)大鼠为空白对照组(WKY空白组)及正常药物对照组(WKY+QD组),SHR+QDH组、SHR+QDL组和SHR+Los组分别经灌胃给予芩丹胶囊及氯沙坦,SHR组和WKY空白组给予等量生理盐水,WKY+QD组给予等量芩丹胶囊灌胃。最后用免疫印迹法和实时定量PCR法检测Ⅰ型胶原的表达水平。结果 WKY空白组、WKY+QD组、SHR+Los组、SHR+QDH组、SHR+QDL组、SHR组Ⅰ型胶原蛋白表达依次增强,SHR+QDH组、SHR+QDL组、SHR+Los组与SHR组比较Ⅰ型胶原蛋白和mRNA表达均显著降低(P<0.05),SHR+QDH组与SHR+Los组比较,差异无统计学意义(P>0.05)。结论芩丹胶囊能有效地降低自发性高血压大鼠血管壁Ⅰ型胶原蛋白与mRNA的表达,改善血管胶原重塑,进而抑制并逆转动脉血管重构。
Objective To observe the effect of Qindan capsule on the expression of collagen Ⅰ and collagen Ⅰ in the vascular wall of aged spontaneously hypertensive rats (SHR) and to explore its mechanism of action on vascular remodeling. Methods Thirty-two aged 40-week-old spontaneously hypertensive rats were randomly divided into three groups: model group (SHR group), high dose QDD group (SHR + QDH group), QDDP group (SHR + QDL group) Losartan group and SHR + Los group, Wistar-Kyoto (WKY) rats were selected as blank control group (WKY blank group) and normal drug control group (WKY + QD group) Rats in QDL group and SHR + Los group were administered with Qindan capsule and losartan respectively by gavage. Rats in SHR group and WKY blank group were given the same amount of normal saline. Rats in WKY + QD group were treated with QDD. Finally, the expression of collagen type Ⅰ was detected by Western blotting and real-time quantitative PCR. Results The expressions of type Ⅰ collagen in WKY blank group, WKY + QD group, SHR + Los group, SHR + QDH group, SHR + QDL group and SHR group were increased in turn. The expression of type Ⅰ collagen in SHR + QDH group, SHR + QDL group, Compared with SHR + Los group, SHR + QDH group showed no significant difference (P> 0.05). There was no significant difference between SHR + QDH group and SHR + Los group (P> 0.05). Conclusion: Qindan Capsule can effectively reduce the expression of type Ⅰ collagen and mRNA in the vascular wall of spontaneously hypertensive rats and improve the remodeling of vascular collagen, and then inhibit and reverse the remodeling of the artery.