细粒棘球蚴囊液抑制脂多糖诱导的巨噬细胞炎症反应

Echinococcus granulosus cyst fluid inhibits the lipopolysaccharide-induced inflammatory response in macrophages through the IL-10/STAT3 signaling

目的观察细粒棘球蚴囊液对脂多糖(LPS)诱导巨噬细胞RAW264.7分泌炎性因子的影响,并探讨其可能的机制。方法培养小鼠巨噬细胞,分为四组处理:对照、囊液(2.15 mg·mL^(-1))、LPS(1μg^(-1) mL^(-1))以及LPS+囊液。刺激5 h后,qRT-PCR检测TNF-α、IL-6和IL^(-1)0的表达;刺激1 h后,免疫印迹法检测STAT3和p-STAT3的蛋白水平。结果囊液能显著抑制LPS诱导的RAW264.7细胞中IL-6和TNF-α的mRNA表达,却明显促进IL^(-1)0的表达。进一步发现囊液能促进STAT3信号的活化水平,而当使用STAT3的抑制剂S3I-201后,STAT3的磷酸化水平明显降低,同时回升了TNF-α的表达。结论细粒棘球蚴囊液能抑制RAW264.7细胞炎症反应,IL^(-1)0/STAT3信号通路可能参与调控此过程。

Objective To observe the effect of Echinococcus granulosus cyst fluid on the secretion of inflammatory cytokines induced by lipopolysaccharide(LPS)in macrophage RAW264.7 cell,and to explore its possible mechanism.Methods Mouse macrophages were cultured and divided into four groups:Control,cyst fluid(2.15 mg·mL^(-1)),LPS(1μg·mL^(-1)),and LPS+cyst fluid.After stimulation for 5 hours,the expression of TNF-α,IL-6 and IL-10 were detected by qRT-PCR.The protein levels of STAT3 and p-STAT3 were detected by Western blot after 1 hour.Results Echinococcus granulosus cyst fluid could dramatically inhibit the LPS-induced mRNA expression of IL-6 and TNF-α,but the expression of IL-10 significantly increased.It was further found that the cyst fluid could promote the activation level of STAT3 signal,however,the phosphorylation level of STAT3 was significantly reduced when the STAT3 inhibitor S3I-201 was used,the expression of TNF-α was also rescued.Conclusion Echinococcus granulosus cyst fluid can inhibit the inflammatory response of RAW264.7 cells,IL-10/STAT3 signaling pathway may be involved in regulating this process.