摘要
目的观察饮用绿茶对大鼠血管钙化的影响及其可能机制。方法用肌注维生素D3和灌胃尼古丁诱导大鼠血管钙化模型。实验分为对照组、钙化组、低剂量和高剂量绿茶干预组。Von Kossa染色,原子吸收分光光度法测定钙含量,放射免疫分析法测定血浆、血管骨钙素(osteocalcin,OC)、血管紧张素Ⅱ(angiotensin II,AngⅡ)及碱性磷酸酶(alkaline phosphatase,ALP)活性。结果钙化组大鼠血管染色见平滑肌细胞内和细胞间基质有大量黑色颗粒聚集;与对照组相比,主动脉钙含量、ALP活性、OC和AngⅡ含量均有明显增加;采用50g/L和100 g/L绿茶防治大鼠均可抑制血管钙化,且高剂量时效应强于低剂量;与钙化组相比较,血管组织钙化指标均下降,而主动脉AngⅡ含量亦有减少。结论饮用绿茶可能部分通过拮抗血浆和血管组织局部的AngⅡ系统效应而产生抑制大鼠血管组织钙化的作用。
Objective To explore the possible mechanism which was involved in the regulatory action of green tea on vascular calcification.Methods Rat vascular calcific model was made by vitamin D3 intramuscular injection and oral nicotine.Rats were divided into four groups:the control,the calcification,lower and higher dosage green tea groups.The total aorta Ca^2+ content in aorta was measured by atom absorptive spectrophotography;the alkaline phosphatase(ALP)activity in plasma and aorta;and the levels of osteocalcin(OC),angiotensin II(Ang Ⅱ)in plasma and aorta were determined by radioimmunoassay.Results A large number of lack granules among the smooth muscle cells and its matrix in calcified aorta by Von Kossa staining in VDN group was observed.More calcium contents,ALP and OC were observed in VDN group than that in control group.AngⅡ level of aortic was significantly increased.The calcification in aorta was significantly attenuated by drinking with green tea 50 g/L and 100 g/L for 6 weeks,and the latter dosage was more potent than the former.After the geen tea treatment,the total aorta Ca^2+ contents,ALP activity,and OC levels were less respectively than those in rats with vascular calcification.Green tea treatment significantly decreased AngⅡ level.Conclusion The results indicated that green tea could significantly attenuate the calcification in rat aorta partly through the antagonism with AngⅡ system in circulation and vascular tissues.group
出处
《宁夏医学院学报》
2008年第4期424-426,F0003,共4页
Journal of Ningxia Medical College
基金
2005年宁夏医学院面上项目(XM200526)
2005年宁夏自然科学基金(NZ0534)
关键词
绿茶
大鼠
血管钙化
血管紧张素Ⅱ
green tea
rat
vascular calcification
angiotensin II