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目的:研究黄芩苷对糖基化终末产物(AGEs)所致的人脐静脉血管内皮细胞株(CRL1730)凋亡的影响。方法:CRL1730细胞常规培养传代,加入不同浓度糖基化终末产物(400mg/L)、黄芩苷(50mg/L、100mg/L、200mg/L)。流式细胞术测定内皮细胞的凋亡率MTT测增殖率,酶联免疫吸附法测sICAM-1、TNF-α。化学法检测NO,黄嘌呤氧化酶法测SOD。结果:黄芩苷能抑制AGEs导致的内皮细胞凋亡,促进增殖率,并同时降低sICAM-1、TNF-α,并升高NO、SOD。结论:黄芩苷对糖基化终末产物导致的CRL1730细胞凋亡的增加、增殖能力下降具有保护作用,其原因可能与其抑制炎症反应等因素有关。
Objective: To study the effects of baicalin on the apoptosis of human umbilical vein endothelial cell line (CRL1730) induced by advanced glycation end products (AGEs). Methods: The CRL1730 cells were passaged routinely. Different concentrations of glycosylation end products (400mg / L) and baicalin (50mg / L, 100mg / L, 200mg / L) were added into the cells. Flow cytometry was used to determine the rate of apoptosis of endothelial cells by MTT assay and sICAM-1 and TNF-α by enzyme-linked immunosorbent assay. Chemical detection of NO, xanthine oxidase method for the determination of SOD. Results: Baicalin could inhibit endothelial cell apoptosis induced by AGEs, promote proliferation, reduce sICAM-1, TNF-α and increase NO and SOD. CONCLUSION: Baicalin has a protective effect on the increase of apoptosis of CRL1730 cells induced by advanced glycation end products and the decrease of proliferative capacity, which may be related to the inhibition of inflammation and other factors.