| 李叶静,谈弋.紫草素通过TLR4/NF-κB信号通路抑制由脂多糖诱导的巨噬细胞炎症研究[J].安徽医药,2017,21(8):1384-1387. |
| 紫草素通过TLR4/NF-κB信号通路抑制由脂多糖诱导的巨噬细胞炎症研究 |
| Anti-inflammatory effects of Shikonin by TLR4/NF-κB pathway to inhibit LPS-induced macrophage inflammatory |
| 投稿时间：2016-09-05 |
| DOI： |
| 中文关键词: 紫草素 腹腔巨噬细胞 炎症细胞因子 Toll样受体4信号通路 |
| 英文关键词: |
| 基金项目: |
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| 中文摘要: |
| 目的 研究紫草素抑制由脂多糖(LPS)诱导的巨噬细胞炎症的机制。方法 以淀粉培养基注射BALB/c小鼠腹腔,诱导并分离巨噬细胞,以APC标记F4/80染色,并用流式细胞仪检测分离巨噬细胞情况；用1 mg·L-1的LPS刺激上述分离的巨噬细胞,分组如下:DMSO溶剂对照组,LPS对照组,LPS+低剂量紫草素组(0.1 μmol·L-1)；LPS+中剂量紫草素组(1 μmol·L-1)；LPS+高剂量紫草素组(10 μmol·L-1)；通过ELISA和实时定量PCR(qRT-PCR)方法分别测定各处理组培养上清液以及细胞中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和白细胞介素-10(IL-10)的表达情况；Western blot分别测定Toll样受体4(TLR4)和核因子-κB(NF-κB)的p65亚基磷酸化表达情况。结果 流式细胞检测可知,APC标记的F4/80染色巨噬细胞的纯度可达97.8%；ELISA和实时定量PCR结果显示,紫草素处理后可以抑制由LPS刺激细胞因子TNF-α、IL-1β和IL-6的表达(P<0.05),并增加IL-10的表达(P<0.05),且呈现出一定的浓度依赖性；Western blot结果显示,紫草素能下调由LPS刺激的TLR4的表达水平和NF-κB的p65亚基磷酸化表达。结论 紫草素的抗炎机制可能是通过TLR4介导的信号通路活化NF-κB,抑制IL-1β、IL-6和TNF-α的分泌,并促进IL-10的分泌。 |
| 英文摘要: |
| Objective Tostudy the roles of Shikonin inhibits LPS-induced macrophage inflammatory andanti-inflammatory effect ofperitoneal macrophages. Methods The peritoneal macrophages of BALB/c mouse were inducedby injectionintraperitoneal mediumand were stained with F4/80.The groupswere divided as follows:DMSO control group,1 mg·L-1 LPS control group,LPS+0.1 μmol·L-1 Shikonin group,LPS+1 μmol·L-1 Shikonin group and LPS+ 10 μmol·L-1 Shikonin group.The levels of TNF-α,IL-1β,IL-6 and IL-10 were detected by ELISA and quantitative real-time PCR method.The expressions of TLR 4 and phosphorylation of p65 (pp65) were measured by Western blot. Results After treatment with shikonin,the expression of TNF-α,IL-1β,IL-6 and IL-10 stimulated by LPSwere decreased(P<0.05),while the expression of IL-10 showed the opposite effect (P<0.05).The expression level of TLR4 and pp65 in peritoneal macrophages stimulated with LPS were inhibited by Shikonin. Conclusion The anti-inflammatory mechanism of shikonin might be mediated by TLR4/NF-κB signaling pathway to inhibit IL-1β,IL-6 and TNF-α and promote the secretion of IL-10. |
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