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目的探讨人参皂苷Re(ginsenoside Re)对球囊损伤所致血管新生内膜增生的作用及其分子机制。方法利用雄性SD大鼠建立球囊损伤致颈动脉内膜增生模型,模型制备完成后后将40只大鼠随机分为5组:人参皂苷Re 6、12、24 mg·kg-1·d-1剂量组、模型组及假手术组,每组8只,术后次日腹腔注射给药,模型组与假手术组给予等体积生理盐水,连续给药14 d后取损伤侧颈动脉行HE染色,观察颈动脉血管腔狭窄程度并计算新生内膜面积及内膜/中膜面积的比值;实时荧光定量聚合酶链反应法检测血管壁丝裂原活化蛋白激酶磷酸酶-1(mitogen-activated protein kinase phosphatase-1,MKP-1)mRNA的表达;免疫组织化学法检测血管壁丝裂原活化蛋白激酶磷酸酶-1和磷酸化细胞外信号调节激酶1/2(phosphorylation extracellular signal-regulated kinase,p ERK1/2)蛋白质的表达。结果与假手术组比较,模型组血管腔明显狭窄(P<0.01),血管壁磷酸化细胞外信号调节激酶1/2蛋白质表达明显上调,而丝裂原活化蛋白激酶磷酸酶-1 mRNA及蛋白质表达却明显下调;人参皂苷Re各给药组均能改善球囊损伤所致的血管狭窄,使血管壁新生内膜面积、新生内膜/中膜面积的比值明显减小(P<0.05),并逆转球囊损伤后磷酸化细胞外信号调节激酶1/2蛋白质表达(P<0.05)和丝裂原活化蛋白激酶磷酸酶-1 mRNA及蛋白质表达(P<0.05,P<0.01)。结论人参皂苷Re可抑制球囊损伤所致的颈动脉狭窄,其分子机制与抑制ERK通路有关。
Objective To investigate the effect of ginsenoside Re on balloon neointimal hyperplasia induced by balloon injury and its molecular mechanism. Methods The model of carotid intima hyperplasia induced by balloon injury was established by using male SD rats. Forty rats were randomly divided into 5 groups: Ginsenoside Re 6, 12, 24 mg · kg -1 · d- 1 dose group, model group and sham operation group, 8 rats in each group were injected intraperitoneally on the next day after operation. The rats in model group and sham operation group were given equal volume of normal saline. After continuous administration for 14 days, The ratio of neointimal area and intima / media area was calculated. The expression of mitogen-activated protein kinase-1 (AChE-1) was detected by real-time fluorescence quantitative polymerase chain reaction protein kinase phosphatase-1, MKP-1) mRNA were detected by immunohistochemistry. The expressions of mitogen-activated protein kinase phosphatase-1 and phosphorylation extracellular signal-regulated kinase 1/2 p ERK1 / 2) protein expression. Results Compared with the sham operation group, the vascular lumen of the model group was significantly stenosed (P <0.01), and the expression of phosphorylated extracellular signal-regulated kinase 1/2 protein was significantly increased in the model group. The mitogen-activated protein kinase phosphatase-1 mRNA and protein (P <0.05). However, the administration of Ginsenoside Re improved the vascular stenosis induced by balloon injury, and the ratio of neointimal area and neointimal / medial area was significantly decreased (P <0.05) (P <0.05) and mitogen-activated protein kinase phosphatase-1 mRNA and protein expression (P <0.05, P <0.01) after balloon injury. Conclusion Ginsenoside Re can inhibit carotid artery stenosis caused by balloon injury, and its molecular mechanism is related to the inhibition of ERK pathway.