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作 者:张代娟[1] 刘江月[1] 王建英[1] ZHANG Daijuan;LIU Jiangyue;WANG Jianying(Pathophysiology Research Office, Wei fang Medical University, Wei fang 261053, China)
机构地区:[1]潍坊医学院病理生理教研室,山东潍坊261053
出 处:《实用医学杂志》2018年第7期1092-1095,共4页The Journal of Practical Medicine
基 金:国家自然科学基金资助项目(编号:8130068);山东省自然科学基金资助项目(编号:ZR2015HL126)
摘 要:目的探讨3,4-二羟基苯乙酮(3,4-DHAP)抑制脂多糖(LPS)诱导小鼠巨噬细胞株(RAW264.7)炎症反应的可能机制。方法常规培养的RAW264.7细胞随机分为正常组(A);LPS组(B);3,4-DHAP组(C)、辛伐他汀组(D)。酶联免疫吸附(ELISA)法检测肿瘤坏死因子(TNF-α)、血管细胞黏附分子(VCAM-1)水平;免疫印迹(Western blot)法检测磷酸化IκB(P-IκB)、总IκB、核因子-κBp65(NF-κBp65)蛋白表达;实时定量荧光聚合酶链式反应(q RT-PCR)法检测IκB mRNA表达。结果 3,4-DHAP显著抑制TNF-α、VCAM-1分泌;抑制IκB蛋白磷酸化;细胞核内NF-κBp65蛋白表达明显减少(P<0.05),抑制了NF-κBp65核转位。结论 3,4-DHAP通过抑制NF-κB核转位,有效抑制LPS诱导RAW264.7细胞炎症反应。Objective To investigate the inhibitory effects and mechanisms of 3,4-dihydroxyacetophe- none (3,4-DHAP) on inflammation induced by lipopolysaccharide (LPS) in murine macrophage cells (RAW264.7). Methods RAW264.7 cell line was cultured and randomly divided into normal group (A) , LPS group (B), 3,4- DHAP group (C) and simvastatin group (D) . The levels of tumor necrosis factor-α (TNF-α) and vascular cell adhesion molecule-1 (VCAM-1) were detected by ELISA kits. The expression of phosphorylation of I kappa B (P-1κB) , total I kappa B (IκB) and NF-κBp65 protein were detected by Western-blotting. qRT-PCR method was used to detect the expression of IKB mRNA. Results After 3,4-DHAP treatment, the levels of TNF-α and VCAM-1 in 3,4-DHAP group were obviously decreased, the expression of P-IκB protein and IκBmRNA and protein increased significantly, and the expression of NF-κBp65 protein in the nuclear were significantly decreased (P〈0.05). Conclusion 3,4-DHAP effectively reduce the inflammatory response induced by LPS through inhibi- tion of NF-κB nuclear translation.
分 类 号:R543.5[医药卫生—心血管疾病]
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