银杏黄素抑制IκB-α的降解缓解LPS诱导的巨噬细胞炎症损伤

Ginkgetin alleviates LPS-induced inflammatory damage in macrophages of mouse model via inhibiting IκB-αdegradation

目的探究天然化合物银杏黄素(Ginkgetin)对脂多糖(LPS)诱导的小鼠腹腔原代巨噬细胞的抗炎作用及其机制,为临床候选药物的开发提供理论依据。方法应用MTT检测试剂盒检测银杏黄素对小鼠腹腔原代巨噬的细胞毒性;运用ELISA、RT-qPCR方法检测不同浓度银杏黄素对LPS诱导的细胞炎症损伤模型的抗炎效果;通过Western blot法检测银杏黄素的抗炎机制。结果与LPS刺激组相比,Ginkgetin治疗组产生了浓度依赖性的抗炎效果,表现于Ginkgetin能显著抑制LPS诱导的IκB-α的降解,而对于LPS诱导的另一经典炎症通路MAPKs信号通路没有影响。MTT结果也表明银杏黄素对小鼠腹腔原代巨噬细胞的毒性较小。结论银杏黄素通过抑制IκB-α的降解从而缓解LPS诱导的小鼠腹腔原代巨噬细胞炎症损伤,有望成为天然单体抗炎候选药物。

Aim To explore the anti-inflammatory effect of natural compound Ginkgetin on lipopolysac-charide-induced mouse primary peritoneal macrophages and the underlying mechanism, in order to provide a theoretical basis for the development of clinical drug candidates. Methods MTT test kit was used to detect the cytotoxicity of Ginkgetin on mouse primary peritoneal macrophages;ELISA and RT-qPCR methods were used to detect the anti-inflammatory effect of different concentrations of Ginkgetin on LPS-induced cell inflammation injury model;Western blot was used to detect the anti-inflammatory mechanism of ginkgo flavonoids. Results Compared with LPS stimulation group, Ginkgetin treatment group produced a concentration-dependent anti-inflammatory effect, which could be attributed to the fact that Ginkgetin could inhibit LPS-induced activation of NF-κB signaling pathway. MTT results also showed that ginkgo flavonoids had little toxicity to mouse primary peritoneal macrophages. Conclusions Ginkgelin alleviates LPS-induced inflammatory injury of mouse primary peritoneal macrophages by inhibiting the activation of NF-κB signaling pathway. It is expected to be a natural monomer anti-inflammatory drug candidate.