黄芩苷对糖基化终末产物所致CRL1730细胞凋亡的影响  

Effect of baicalin on apoptosis and proliferation of CRL1730 cells exposed to advanced glycationend products

作　　者：曾敬[1] 王静[2] 张蕾[1] 张海燕[1] 唐俊明[2] 王家宁[2] 

机构地区：[1]湖北郧阳医学院附属人民医院,十堰442000 [2]郧阳医学院预防教研室,十堰442000

出　　处：《中药药理与临床》2010年第3期13-15,共3页Pharmacology and Clinics of Chinese Materia Medica

基　　金：湖北省教育厅基金项目(B200724007)

摘　　要：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 investigate the effect of baicalin on proliferation,apoptosis in cultured human umbilical vein endothelial cells（CRL1730）exposed to advanced glycation end products.Methods：The cultured CRL1730 exposed to advanced glycation end products（400mg/L） were treated with baicalin （50mg/L,100mg/L,200mg/L）for 48 hours.Proliferation and apoptosis of CRL1730 were evaluated by MTT assay,flow eytometry（FCM）,soluble intercellular adhesion molecule-1 （sICAM-1）,tumor necrosis factor-α （TNF-α） were measured by ELESA,nitric oxide was measured by colorimetry and xanthine oxidase test activity of superoxide dismutase（SOD）.Results：Under advanced glycation end products apoptosis rate of baicalin groups declined,and the proliferation escalate.At the same time,the sICAM-1 and TNF-α decreased and vitality of SOD and NO increased.Conclusion：Under the condition of advanced glycation end products,baicalin can correct the increase of apoptosis rate,abnormal change of the inhibition of proliferation.The cause is that baicalin may inhibit inflammatory response and oxidative stress.

关 键 词：黄芩苷 人脐静脉血管内皮细胞株 糖基化终末产物 凋亡 

分 类 号：R285[医药卫生—中药学]