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目的:对比观察冠心康和锌对镉染毒人脐静脉内皮细胞NO水平和细胞增殖率的变化,分析其抗镉染毒致动脉粥样硬化的可能途径。方法:人脐静脉内皮细胞体外培养,随机分为空白组、模型组、补锌组,及冠心康低、中、高剂量组,分别以空白血清、CdCl2血清、CdCl2及硫酸锌血清和CdCl2及冠心康血清培养24h、48h、72h,收集培养液,硝酸还原酶法测定NO浓度,MTT法检测细胞增值率;结果:1μM、5μM、10μM、30μM和60μM各组镉染毒HUVECS细胞NO水平明显下降(P<0.01),60μΜ镉染毒浓度可致HUVECs细胞增殖率(PR)显著降低(P<0.01);而与模型组相比,冠心康组、补锌组的NO含量和PR均有明显恢复(P<0.01)。结论:①冠心康可明显提高镉染毒HUVECs的NO和PR,从而减少血管内皮损伤,发挥抗动脉粥样硬化作用;②气虚痰瘀可能是镉染毒诱发动脉硬化的主要病机。
OBJECTIVE: To observe the changes of NO level and cell proliferation rate induced by cadmium in human umbilical vein endothelial cells treated with Guanxinkang and zinc, and to analyze the possible pathways of coronary heart disease and atherosclerosis induced by cadmium exposure. Methods: Human umbilical vein endothelial cells were cultured in vitro and randomly divided into blank group, model group, zinc supplementation group and low and medium dose Guanxinkang group. The serum, CdCl2 serum, CdCl2 and zinc sulfate serum and CdCl2 And Guanxinkang serum were cultured for 24h, 48h, 72h. The concentration of NO was determined by nitrate reductase method and the cell proliferation rate was measured by MTT assay. Results: The cell proliferation rate was significantly increased in the cells exposed to cadmium at 1μM, 5μM, 10μM, 30μM and 60μM (P <0.01). The cell proliferation rate (PR) of HUVECs induced by cadmium at a concentration of 60μM was significantly lower than that of the model group (P <0.01) PR were significantly recovered (P <0.01). Conclusion: Guanxinkang can significantly increase NO and PR of cadmium-exposed HUVECs, thereby reducing vascular endothelial injury and exerting anti-atherosclerotic effects; ② Qi-deficiency and phlegm-stasis syndrome may be the main pathogenesis of atherosclerosis induced by cadmium exposure.