Objective To observe the anti-inflammatory effects of Kangfuxin in cell inflammation of macrophages and to discuss the possible mechanism .Methods The cultivated mouse macrophages RAW 264 .7 were randomly divided into 6 groups:group A ( added with DMSO ) , group B ( added with DMSO ) , group C ( added with anti-inflammation drug BAY11-7082), group D (added with 1%Kangfuxin), group E (added with 0.1%Kangfuxin), and group F (added with 0.01%Kangfuxin).We continued to cultivate for 1 h after drug intervention, group A was treaded with DMEM, the other groups were treated with LPS (100 μg/L) to induce cell inflammation.The cells were collected after treatment of 4 h and 8 h, the mRNA expression levels of IL-6, TNF-αand prostaglandin-endoperoxide synthase ( PTGS2) were detected by qRT-PCR.Results Four hours and eight hours after modeling , compared with group A , the mRNA expression levels of IL-6, TNF-αand PTGS2 were increased in the group B (all P<0.05); compared with group B, the mRNA expression levels of IL-6, TNF-αand PTGS2 were decreased in the group C (all P<0.05).All cells were dead in the group D.Com-pared with group B , the mRNA expression of IL-6 and TNF-αwas increased and the PTGS 2 mRNA expression was de-creased in the groups E and F (all P<0.05).Compared with group C, significant difference was found in the mRNA ex-pression of IL-6 and TNF-αbetween groups E and F (all P<0.05), and no significant difference was found in the mRNA expression of PTGS2 between groups E and F (all P>0.05).The concentration and duration of Kangfuxin had no effect on the mRNA expression of IL-6, TNF-αand PTGS2.Conclusion Kangfuxin has inhibitory effect on the cell inflammatory reaction, and its mechanism may be not related with the inhibition of expression of inflammatory factors , such as IL-6 and TNF-α, but be related with the down-regulated PTGS2 expression.%目的 观察康复新在巨噬细胞炎症反应中的抗炎作用,并探讨其可能的作用机制.方法 将培养好的小鼠巨噬细胞RAW264.7随机分为6组:A组(加入DMSO)、B组(加入DMSO)、C组(加入炎症抑制药物BAY11-7082)、D组(加入1%康复新)、E组(加入0.1%康复新)、F组(加入0.01%康复新),药物干预后继续培养1 h,A组加DMEM培养液,其余各组加入LPS(100μg/L)诱导细胞产生炎症反应.造模后4、8 h收集细胞,用qRT-PCR法检测细胞中白细胞介素(IL)6、肿瘤坏死因子(TNF)α、前列腺素内过氧化物合酶(PTGS)2的mRNA表达.结果造模后4、8 h,与A组比较,B组IL-6、TNF-α、PTGS2的mRNA表达水平均升高(P均<0.05);与B组比较,C组IL-6、TNF-α、PTGS2的mRNA表达均降低(P均<0.05).D组在收集细胞时即观察到细胞全部死亡.与B组比较,E、F组IL-6、TNF-α的mRNA表达升高,PTGS2的mRNA表达降低(P均<0.05);与C组比较,E、F组IL-6、TNF-α的mRNA表达差异有统计学意义(P均<0.05),而PTGS2的mRNA表达差异无统计学意义(P均>0.05).康复新的浓度、作用时间对IL-6、TNF-α、PTGS2的mRNA表达无影响.结论 康复新对巨噬细胞炎症反应有抑制作用,该作用不是通过抑制IL-6、TNF-α等致炎因子的表达,而是与降低PTGS2的表达有关.
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