KCa3.1在藏红花素促进人脐静脉内皮细胞NO生成过程中的调节作用

Role of KCa3.1 in NO generation promoted by crocin in HUVECs

目的观察藏红花素(crocin)对人脐静脉内皮细胞(HUVECs)体外eNOS表达及NO生成的影响以及。方法用crocin及KCa3.1选择性阻断剂tram34分别处理HUVECs,NO荧光探针DAF-FM DA检测HUVECs细胞中NO的表达, Western blot法检测磷酸化一氧化氮合酶(peNOS)和总一氧化氮合酶(t-eNOS)的表达。结果 crocin明显促进细胞内NO的生成,提高p-eNOS和t-eNOS蛋白的表达水平;在KCa3.1选择性阻断剂tram34的干预下,crocin对于HUVECs中NO及eNOS的上调作用被明显抑制。结论藏红花素促进内皮细胞eNOS介导的NO生成与KCa3.1信号通路相关。

Objective To observe the effect of crocin on eNOS and NO production as well as the regulation of KCa3.1 in human umbilical vein endothelial cells(HUVECs).Methods HUVECs were treated with crocin and/or tram34,a selective inhibitor of calcium-activated potassium channel(KCa3.1).DAF-FM DA,a probe for NO was used to examine the effect of crocin on NO generation in HUVECs.Furthermore,the expressions of phosphorylated nitric oxide synthase(peNOS)and total nitric oxidesynthase(t-eNOS)were detected by Western blot.Results Crocin significantly promoted the production of NO and the expression levels of p-eNOS and t-eNOS.However,the inhibitor tram34 could reduce the crocinupregulated expression of p-eNOS and t-eNOS.Conclusion Crocin promoted eNOS mediated NO production in endothelial cells via KCa3.1 signaling pathway.