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作 者:胡为杰 易祎 熊铭琛 赵崇茹 吴毅平[1] 罗晓[1] Hu Weijie;Yi Yi;Xiong Mingchen;Zhao Chongru;Wu Yiping;Luo Xiao(Department of Plastic Surgery,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China)
机构地区:[1]华中科技大学同济医学院附属同济医院整形美容外科,武汉430030
出 处:《中华实验外科杂志》2020年第8期1461-1463,共3页Chinese Journal of Experimental Surgery
摘 要:目的探讨柯里拉京(Corilagin)对小鼠巨噬细胞RAW264.7的M2型极化和纤溶相关细胞因子[白细胞介素(IL)-10和基质金属蛋白酶(MMP)-9]表达的影响。方法取RAW264.7细胞系(中乔新舟生物科技有限公司)分为6组:M0型对照组、M0型低浓度(4 mg/L)Corilagin组、M0型高浓度(32 mg/L)Corilagin组、M2型极化组、M2型极化低浓度(4 mg/L)Corilagin组和M2型极化高浓度(32 mg/L)Corilagin组,分组培养24 h,采用实时荧光定量聚合酶链反应(Real-time PCR)检测M2型巨噬细胞标识分子和纤溶相关细胞因子的mRNA表达水平。各组间比较采用单因素方差(One-way ANOVA)和t检验。结果高浓度Corilagin(32 mg/L)处理后RAW264.7细胞的M2型极化标识分子CD206、Arg-1和Fizz1的mRNA表达水平分别为33.61±1.36(F=24.990,P<0.05)、3.74±0.73(F=73.100,P<0.01)和2.25±0.74(F=11.100,P<0.01);同时,高浓度Corilagin处理的M2型巨噬细胞的纤溶相关细胞因子IL-10和MMP-9的相对表达量分别为1.53±0.30(F=7.150,P<0.05)和1.37±0.05(F=53.950,P<0.01)。结论Corilagin可能通过抑制巨噬细胞M2型极化、影响M2型巨噬细胞的亚型分布和促进纤溶相关细胞因子表达,参与伤口愈合的病理生理过程。Objective To observe the effect of corilagin on the M2 macrophage polarization and fibrinolysis-related cytokines[interleukin(IL)-10 and matrix metalloproteinase(MMP)-9]expression in mouse macrophage RAW264.7.Methods The RAW264.7 cell line induced by IL-4 was treated with corilagin in a low concentration(4 mg/L)or a high concentration(32 mg/L)for 24 hours,using real-time fluorescence quantitative polymerase chain reaction(PCR)to detect the mRNA expression of marker molecules and fibrinolysis-related cytokines.Results After treatment with high concentration of Corilagin(32 mg/L),the relative expression of M2 polarization marker molecules CD206,Arg-1 and Fizz1 were 33.61±1.36(F=24.990,P<0.05),3.74±0.73(F=73.100,P<0.01)and 2.25±0.74(F=11.100,P<0.01).Meanwhile,the relative expression levels of fibrinolysis-related cytokines IL-10 and MMP-9 in M2 macrophages treated with high concentration of Corilagin were 1.53±0.30(F=7.150,P<0.05)and 1.37±0.05(F=53.950,P<0.01).Conclusion Corilagin may affect the pathophysiological process of wound healing by inhibiting M2 macrophage polarization,affecting the subtype distribution of M2 macrophages,and promoting the expression of fibrinolysis-related cytokines.
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