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作 者:高爱社[1] 杨洒 孙续鹏 刘亚美[1] 张妍[1] 陈芳[1] GAO Aishe;YANG Sa;SUN Xupeng;LIU Yamei;ZHANG Y an;CHEN Fang(Henan University of Chinese Medicine,Zhengzhou Henan China 450046)
机构地区:[1]河南中医药大学
出 处:《中医学报》2019年第12期2597-2600,共4页Acta Chinese Medicine
基 金:河南省科技攻关计划项目(162102310182);河南省高等学校重点科研项目(20A310009)
摘 要:目的:观察丹参酮ⅡA对β淀粉样蛋白(Aβ1-42)诱导的脑微血管内皮细胞(brain microvascular endothelial cell,BMEC)损伤模型活性的影响。方法:建立Aβ1-42致BMEC损伤模型,用不同质量浓度(10 mg·L^-1、30 mg·L^-1、50 mg·L^-1)的丹参酮ⅡA干预,MTT法检测细胞活性,微板法检测上清液中乳酸脱氢酶(lactate dehydrogenase,LDH)水平,Western blot法检测核因子-κB(nuclear factor-κB,NF-κB)相关蛋白表达结果。结果:与模型组比较,丹参酮ⅡA的3个剂量组BMEC活力显著升高(P<0.05)。与模型组比较,丹参酮ⅡA的3个剂量组LDH活性显著降低(P<0.05)。与模型组比较,丹参酮ⅡA的3个剂量组NF-κB p65蛋白表达显著减低,IKB-α蛋白表达显著升高,差异均有统计学意义(P<0.05)。与模型组比较,丹参酮ⅡA的3个剂量组NF-κB p65磷酸化表达水平显著降低(P<0.05)。结论:丹参酮ⅡA能提高Aβ1-42致BMEC损伤模型的BMEC的活力,降低LDH活性、NF-κB p65蛋白表达、NF-κB p65磷酸化表达水平,升高IKB-α蛋白表达。Objective:To observe the effect of tanshinone IIA on the activity of β-amyloid protein(Aβ1-42)-induced brain microvascular endothelial cell(BMEC) injury model.Methods:Aβ1-42-induced BMEC injury model was established.Tanshinone IIA with different concentrations(10 mg·L^-1,30 mg·L^-1,50 mg·L^-1) was used to intervene.Cell viability was detected by MTT assay.The levels of lactate dehydrogenase(LDH) in serum were detected by Western blot.The expression of nuclear factor-κB(NF-κB)-related protein was detected by Western blot.Results:Compared with the model group,the BMEC activity of the three doses of tanshinone IIA was significantly increased(P<0.05).Compared with the model group,the LDH activity of the three dose groups of tanshinone IIA was significantly lower(P<0.05).Compared with the model group,the expression of NF-κB p65 protein in the three dose groups of tanshinone IIA was significantly decreased,and the expression of IKB-α protein was significantly increased(P<0.05).Compared with the model group,the expression level of NF-κB p65 phosphorylation was significantly decreased in the three dose groups of tanshinone IIA(P<0.05).Conclusion:Tanshinone IIA can increase the activity of BMEC in Aβ1-42-induced BMEC injury model,decrease LDH activity,NF-κB p65 protein expression,NF-κB p65 phosphorylation expression,and increase IKB-α protein expression.
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