详细信息

藁本内酯对血管紧张素Ⅱ诱导损伤的人脐静脉内皮细胞中miR-122表达的影响及其作用机制    

Effect of ligustilide on expression of miR-122 in injured human umbilical vein endothelial cells induced by angiotensinⅡ

文献类型:期刊文献

中文题名:藁本内酯对血管紧张素Ⅱ诱导损伤的人脐静脉内皮细胞中miR-122表达的影响及其作用机制

英文题名:Effect of ligustilide on expression of miR-122 in injured human umbilical vein endothelial cells induced by angiotensinⅡ

作者:杨锐[1];谢青[1];江华[1];毛玉娟[1];王莉[1];何亚丽[1];申进增[1];伊琳[1]

第一作者:杨锐

机构:[1]甘肃中医药大学中西医结合学院,甘肃兰州730000

第一机构:甘肃中医药大学中西医结合学院

年份:2021

卷号:34

期号:6

起止页码:678

中文期刊名:中国生物制品学杂志

外文期刊名:Chinese Journal of Biologicals

收录:CSTPCD;;Scopus;北大核心:【北大核心2020】;CSCD:【CSCD_E2021_2022】;

基金:国家自然科学基金(81760803);甘肃中医药大学研究生创新基金(2019CX19)。

语种:中文

中文关键词:藁本内酯;血管紧张素Ⅱ;miR-122;人脐静脉内皮细胞

外文关键词:Ligustilide;AngiotensinⅡ(AngⅡ);miR-122;Human umbilical vein endothelial cells(HUVECs)

摘要:目的探讨藁本内酯对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导的人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)中miR-122表达的影响及其作用机制。方法将HUVECs随机分为6组:空白组(不给药)、模型组(1×10^(-5)mol/L AngⅡ)、缬沙坦组(1×10^(-5)mol/L AngⅡ+1×10^(-4)mol/L缬沙坦)及藁本内酯低剂量组(1×10^(-5)mol/L AngⅡ+1×10^(-5)mol/L藁本内酯)、中剂量组(1×10^(-5)mol/L AngⅡ+1×10^(-4)mol/L藁本内酯)、高剂量组(1×10^(-5)mol/L AngⅡ+1×10-3mol/L藁本内酯)。CCK8法检测各组细胞的细胞活性,NO检测试剂盒检测各组细胞培养基上清液中NO水平,RT-qPCR检测各组细胞中miR-122表达及阳离子氨基酸转运体1(solute carrier family 7 member 1,Slc7a1)基因mRNA的转录水平,Western blot法检测各组细胞中阳离子氨基酸转运蛋白-1(cationic amino acid transporter-1,CAT-1)水平。结果与空白组比较,模型组HUVECs中miR-122表达水平明显升高(P<0.01),细胞活性、NO、Slc7a1基因mRNA转录及CAT-1表达水平均明显降低(P<0.01)。与模型组比较,缬沙坦组及藁本内酯低、中、高剂量组miR-122表达水平明显降低(P<0.01),细胞活性、NO及CAT-1表达水平均明显升高(P<0.01);缬沙坦组及藁本内酯中、高剂量组Slc7a1基因mRNA转录水平明显升高(P<0.01)。结论藁本内酯可抑制AngⅡ诱导损伤HUVECs中miR-122的表达,其作用机制可能与miR-122/CAT-1/NO通路相关。
Objective To investigate the effect of ligustilide on expression of miR-122 in injured human umbilical vein endothelial cells(HUVECs)induced by angiotensinⅡ(AngⅡ)as well as the relevant mechanism.Methods HUVECs were randomly divided into six groups,i.e.blank control(untreated),model(1×10^(-5) mol/L AngⅡ),valsartan(1×10^(-5) mol/L AngⅡ+1×10^(-4) mol/L valsartan)as well as low(1×10^(-5) mol/L AngⅡ+1×10^(-5) mol/L ligustilide),moderate(1×10^(-5) mol/L AngⅡ+1×10^(-4) mol/L ligustilide)and high dose ligustilide(1×10^(-5) mol/L AngⅡ+1×10-3 mol/L ligustilide)groups.The cell viabilities in various groups were determined by CCK8 method,while the nitric oxide(NO)level in culture supernatant by NO detection kit,the miR-122 expression and solute carrier family 7 member 1(Slc7a1)mRNA transcription level by RT-qPCR,and the expression level of cationic amino acid transporter protein-1(CAT-1)by Western blot.Results Compared with those in blank control group,the expression level of miR-122 in model group increased significantly(P<0.01),while the cell viability,NO and Slc7 a`mRNA transcription level as well as CAT-1 expression level decreased significantly(P<0.01).Compared with those in model group,the expression levels of miR-122 in valsartan as well as low,moderate and high dose ligustilide groups decreased significantly(P<0.01),while the cell viability as well as NO and CAT-1 expression levels increased significantly(P<0.01).However,the Slc7a1 mRNA transcription levels in valsartan as well as low and moderate dose ligustilide groups increased significantly(P<0.01).Conclusion Ligustilide inhibited the miR-122 expression in injured HUVECs induced by AngⅡby a mechanism which might be associated with miR-122/CAT-1/NO pathway.

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