CAJ | 학술논문

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畅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畅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。
목적：탐토은행협제취물（EGb）대지다당（LPS）유도적C6세포염증인자표체적영향급p38MAPK적작용。방법 C6세포배양，가입LPS급 EGb예처리，ELISA법측정상청 TNF －α적함량；진일보분위LPS、EGB＋LPS、EGb＋ LPS＋ anisomycin、공백대조조4조，ELISA법측정상청 TNF－α적함량；Western－blot법검측린산화p38화IL －1단백적표체；RT －PCR법검측p38mRNA화IL－1mRNA적표체。결과가입불동농도적 LPS 처리후，TNF －α적표체명현고우대조조（P ＜0창001）；불동농도적EGb예처리후，TNF －α적표체명현저우 LPS조（P ＜0．01，P ＜0．001）；가입EGb、anisomycin 예처리후，TNF －α적표체명현고우 EGb 예처리조（P ＜0．001）。LPS 조적p38MAPK、IL －1적단백질화mRNA적표체명현고우대조조（P＜0．001），EGb예처리조교LPS조표체감소（P ＜0．001），격활 p38통로후，EGb、anisomycin예처리조표체고우 EGb예처리조（P ＜0창001）。결론 EGb가능통과억제p38통로억제TNF－α、IL －1적표체，억제염증반응。
Objective To investigate the effet of Ginkgo biloba extract (EGb) on inflammatory cyto‐kines 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 phosphoryl‐ation 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 reac‐tion by inhibiting expression of TNF-αand IL -1 through inhibiting the p38 pathway .