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二甲双胍对LPS诱导THP-1细胞所产生的相关炎症因子的影响 被引量:5

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摘要 目的通过反转录聚合酶链反应(RT-PCR)技术,检测在二甲双胍(Met)及腺苷酸活化蛋白激酶(AMPK)的阻断剂复合物C(compound C)干预下,脂多糖(LPS)诱导的人单核细胞(THP-1)相关炎症因子白介素1β(IL-1β)、肿瘤坏死因子(TNF-α)基因水平的表达,探讨Met的抗炎作用及抗炎机制。方法体外培养人单核细胞,并分为对照组,LPS组(1μg/mL LPS),Met组(Met 5mmol/L+LPS 1μg/mL),复合物C组(Met 5mmol/L+LPS 1μg/mL+compound C 10μmol/L)分别孵育6h后,提取细胞进行检测。台盼蓝染色镜下计数观察细胞存活率。RT-PCR检测细胞炎症因子IL-1β、TNF-α的表达水平。结果 Met在干预6h后,可降低LPS所诱导的THP-1细胞的炎症因子IL-1β、TNF-α的基因表达。Met组炎症因子IL-1β、TNF-α的分泌显著低于LPS组(P<0.01)。复合物C组炎症因子IL-1β、TNF-α较Met组表达增加(P<0.01)。结论 Met干预6h可降低LPS诱导的THP-1细胞相关炎症因子IL-1β、TNF-α的基因表达,提示二甲双胍在基因水平上有一定的抗炎作用,且其抗炎途径与激活AMPK有关。
出处 《中西医结合心脑血管病杂志》 2014年第6期737-739,共3页 Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease
基金 国家自然科学基金资助项目(No.81270882)
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同被引文献75

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