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目的:观察赤芍对高脂喂养兔颈动脉球囊损伤后丝裂素活化蛋白激酶磷酸酶-1(MKP-1)mRNA表达、血管紧张素Ⅱ(AgⅡ)激活及内膜增殖的影响。方法:新西兰白兔随机分为对照及赤芍组,各组均饲喂高脂饲料(普通饲料+2%胆固醇+5%猪油)。赤芍组按剂量给予赤芍提取物,高、中、低剂量组相当于生药75、50、25g.kg-1.d-1。球囊损伤颈总动脉内膜建立模型,放射免疫测定血浆AgⅡ水平、测定血管张力、免疫组化染色及形态学测定、RT-PCR检测MKP-1 mRNA表达。结果:与对照组比较,赤芍组AgⅡ水平降低(P<0.05);血管对AgⅡ的收缩反应减弱(P<0.05);增生内膜面积、增生内膜面积/中膜面积显著减少(P<0.05或P<0.01);MKP-1 mRNA表达显著增高(P<0.05或P<0.01)。结论:赤芍降低血浆中的AgⅡ水平,减低血管环对AgⅡ的收缩反应性,增加高脂喂养兔颈动脉球囊损伤后MKP-1 mRNA表达,并减轻内膜增殖程度。表明内膜增殖程度的减低与赤芍抑制RAS激活,并阻断MAPK信号通路有关。
OBJECTIVE: To observe the effects of radix paeoniae on mitogen-activated protein kinase phosphatase-1 (MKP-1) mRNA expression, activation of angiotensin II (Ag II) and intimal hyperplasia after high-fat feeding of rabbit carotid artery. METHODS: New Zealand white rabbits were randomly divided into control and Chishao groups. All groups were fed high-fat diet (ordinary feed + 2% cholesterol + 5% lard). The Radix Paeoniae Alba group was given dose of Radix Paeoniae Rubra extract. The high-, medium-, and low-dose groups were equivalent to crude drugs 75, 50, 25 g.kg-1.d-1. A model of carotid artery intima was established by balloon injury. Plasma Ag II levels were measured by radioimmunoassay, vascular tone was measured, immunohistochemical staining and morphological measurements, and MKP-1 mRNA expression was detected by RT-PCR. RESULTS: Compared with the control group, the level of Ag II in the Chishao group was decreased (P<0.05); the contraction response of the blood vessels to AgII was weakened (P<0.05); the area of proliferative intima and the area of hyperplastic intima/media area were significantly reduced (P< 0.05 or P<0.01); MKP-1 mRNA expression was significantly increased (P<0.05 or P<0.01). Conclusion: Radix Paeoniae Rubra could reduce the level of Ag II in plasma, reduce the contractile reactivity of vascular rings to Ag II, increase the expression of MKP-1 mRNA and reduce the degree of intimal proliferation after high-fat feeding rabbit carotid balloon injury. It is suggested that the reduction of intimal proliferation is related to the suppression of RAS activation by erythra and the blocking of MAPK signaling pathway.