尼氟灭酸对氯化钴诱导血管内皮细胞凋亡的保护作用

Protective effects of Niflumic acid on apoptosis of vascular endothelial cell induced by Cobalt Chloride

目的探讨尼氟灭酸(NFA)对氯化钴(CoCl_2)诱导血管内皮细胞凋亡的保护作用,阐明其可能的机制。方法将血管内皮细胞随机分为对照组、100μmol/L CoCl_2损伤组和20、40μmol/L NFA保护组,四甲基偶氮唑蓝比色(MTT)法检测各组细胞增殖活性,酶联免疫吸附试验(ELISA)检测细胞内相关凋亡蛋白Bcl-2、Bax及Caspse-3的表达情况。结果 MTT检测,与对照组比较,100μmol/L CoCl_2组在24 h细胞增殖活性明显降低(P<0.01);与CoCl_2损伤组相比,20、40μmol/L NFA保护组在24 h细胞增殖活性升高(P<0.05,P<0.01),40μmol/L NFA保护组更加明显。ELISA法检测显示,与对照组比较,100μmol/L CoCl_2组在24 h细胞Caspse-3、Bax的表达增多,Bcl-2表达减少(P<0.05,P<0.01)。与损伤组相比,NFA处理缺氧后血管内皮细胞Caspse-3、Bax的表达减少,Bcl-2表达增多(P<0.05,P<0.01)。结论 CoCl_2能诱导血管内皮细胞缺氧损伤,引起细胞的凋亡;NFA可以保护CoCl_2诱导的血管内皮细胞的缺氧损伤,这可能与上调Bcl-2、下调Bax和Caspse-3抑制其凋亡有关。

Objective To explore the effects of Niflumic acid on the apoptosis of vascular endothelial cells induced by CoCl2 ,and elucidate its mechanisms .Methods Vascular endothelial cells were cultured and randomly divided into control group,100 μmol/L CoCl2 injury group and 20,40 μmol/L NFA groups.The cell proliferation was meas-ured by MTT assay ,and ELISA method was performed to observe the expression of apoptosis associated protein Bax , Bcl-2 and Caspse-3.Results Compared with control group ,the proliferation of vascular endothelial cells was de-creased in 100 μmol/L CoCl2 injury group （P〈0.01）.Compared with 100μmol/L CoCl2 injury group,the prolifera-tion of vascular endothelial cells were increased significantly in 20 and 40μmol/L NFA groups ,and the effect was bet-ter in 40 μmol/L NFA group （P〈0.05,P〈0.01）.The ELISA results showed that the expression of Caspse-3 and Bax in 100 μmol/L CoCl2 injury group were increased ,while the expression of Bcl-2 was reduced compared with con-trol group （P〈0.05,P〈0.01）.Compared with CoCl2 injury group,the expression of Bcl-2 was increased,while the expression of Caspse-3 and Bax were decreased in 40 μmol/L NFA group（P〈0.05,P〈0.01）.Conclusion NFA could protect vascular endothelial cells from hypoxia injury induced by CoCl 2 ,which may be related to down-regulating the expression of Bax and Caspse-3,while up-regulating the expression of Bcl-2 and suppressing apoptosis of vascular endothelial cells .