p38MAPK介导银杏叶提取物对脂多糖诱导C6细胞炎症因子表达的影响

Efects of p38MAPK mediates Ginkgo biloba extract on inflammatory factor expression in C6 cells induced by lipopolysaccharide

目的：探讨银杏叶提取物（EGb）对脂多糖（LPS）诱导的C6细胞炎症因子表达的影响及p38MAPK的作用。方法 C6细胞培养，加入LPS及 EGb预处理，ELISA法测定上清 TNF －α的含量；进一步分为LPS、EGB＋LPS、EGb＋ LPS＋ anisomycin、空白对照组4组，ELISA法测定上清 TNF－α的含量；Western－blot法检测磷酸化p38和IL －1蛋白的表达；RT －PCR法检测p38mRNA和IL－1mRNA的表达。结果加入不同浓度的 LPS 处理后，TNF －α的表达明显高于对照组（P ＜0.001）；不同浓度的EGb预处理后，TNF －α的表达明显低于 LPS组（P ＜0．01，P ＜0．001）；加入EGb、anisomycin 预处理后，TNF －α的表达明显高于 EGb 预处理组（P ＜0．001）。LPS 组的p38MAPK、IL －1的蛋白质和mRNA的表达明显高于对照组（P＜0．001），EGb预处理组较LPS组表达减少（P ＜0．001），激活 p38通路后，EGb、anisomycin预处理组表达高于 EGb预处理组（P ＜0.001）。结论 EGb可能通过抑制p38通路抑制TNF－α、IL －1的表达，抑制炎症反应。

Objective To investigate the effet of Ginkgo biloba extract （EGb） on inflammatory cytokines expression in C6 cells induced by lipopolysaccharide （LPS） and the effect of p38MAPK .Methods C6 cells were cultured ,adding LPS and EGb pretreatment and determination of content of supernatant of TNF -αby ELISA method;further divided into LPS ,EGB＋LPS ,EGb＋LPS＋anisomycin ,four blank control groups ,determination of content of supernatant of TNF-αby ELISA method;The phosphorylation of p38 and IL -1 protein expression were investigated by Western-blot method;the expression of p38mRNA and IL -1mRNA were detected by the RT -PCR method .Results The expression of TNF-αwas significantly higher than that of the control group （P 〈 0 .001） after treatment with different con‐centrations of LPS ;the expression of TNF -α was significantly lower than that of LPS group （P 〈0.01 ,P 〈 0 .001） after pretreatment of different concentrations of EGb;the expression of TNF-α was higher than that in EGb pretreatment group （P 〈 0 .001） after pretreatment of accession with the EGb andanisomycin .Expression of p38MAPK ,IL -1 protein and mRNA were higher in the LPS group than that of control group （P 〈 0 .001） and were decreased in EGb pretreatment group than in LPS group （P 〈0.001） ,and was higher in EGb and anisomycin pretreatment group than that in EGb pretreatment group after activation of the p38 pathway （P〈 0 .001） .Conclusions EGb maybe inhibit the inflammatory reaction by inhibiting expression of TNF-αand IL -1 through inhibiting the p38 pathway .