Zhang Zhenbiao, Guo Yingfang, Liu Yuzhu, Li Chengye, Guo Mengyao, Deng Ganzhen
Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China.
Biomed Res Int. 2017;2017:2350482. doi: 10.1155/2017/2350482. Epub 2017 Feb 26.
The aim of the present study was to determine the anti-inflammatory effect of IFN- on endometritis using a mouse model of -induced endometritis and to elucidate the mechanism of action underlying these effects. In the present study, the effect of IFN- on growth was monitored by turbidimeter at 600 nm. IFN- did not affect growth. The histopathological changes indicated that IFN- had a protective effect on uterus tissues with infection. The ELISA and qPCR results showed the production of the proinflammatory cytokines TNF-, IL-1, and IL-6 was decreased with IFN- treatment. In contrast, the level of the anti-inflammatory cytokine IL-10 was increased. We further studied the signaling pathway associated with these observations, and the qPCR results showed that the expression of TLR2 was repressed by IFN-. Furthermore, the western blotting results showed the phosphorylation of IB, NF-B p65, and MAPKs (p38, JNK, and ERK) was inhibited by IFN- treatment. The results suggested that IFN- may be a potential drug for the treatment of uterine infection due to or other infectious inflammatory diseases.
本研究的目的是使用诱导性子宫内膜炎小鼠模型确定干扰素-对子宫内膜炎的抗炎作用,并阐明这些作用背后的作用机制。在本研究中,通过在600nm处使用比浊计监测干扰素-对生长的影响。干扰素-不影响生长。组织病理学变化表明,干扰素-对感染子宫组织具有保护作用。酶联免疫吸附测定(ELISA)和定量聚合酶链反应(qPCR)结果显示,经干扰素-处理后,促炎细胞因子肿瘤坏死因子-α(TNF-α)、白细胞介素-1(IL-1)和白细胞介素-6(IL-6)的产生减少。相反,抗炎细胞因子白细胞介素-10(IL-10)的水平升高。我们进一步研究了与这些观察结果相关的信号通路,qPCR结果显示,干扰素-可抑制Toll样受体2(TLR2)的表达。此外,蛋白质印迹结果显示,经干扰素-处理后,IκB、核因子-κB p65(NF-κB p65)和丝裂原活化蛋白激酶(MAPKs,包括p38、c-Jun氨基末端激酶(JNK)和细胞外信号调节激酶(ERK))的磷酸化受到抑制。结果表明,干扰素-可能是治疗因或其他感染性炎症疾病引起的子宫感染的潜在药物。