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飞扬肠胃炎胶囊通过JNK/NF-κB通路对大鼠盆腔炎的抗炎作用

Anti-Inflammatory Effect of Feiyangchangweiyan Capsule on Rat Pelvic Inflammatory Disease through JNK/NF-B Pathway.

作者信息

Li Yao, Liu Yang, Yang Qian, Shi Zhihui, Xie Yanhua, Wang Siwang

机构信息

School of Pharmacy, Shaanxi University of Chinese Medicine, Xianyang 712000, China.

College of Chemistry and Pharmacy, Northwest Agriculture and Forestry University, Yangling 712100, China.

出版信息

Evid Based Complement Alternat Med. 2018 Feb 28;2018:8476147. doi: 10.1155/2018/8476147. eCollection 2018.

Abstract

OBJECTIVES

In this study, we aimed to illustrate the preventive effect and possible mechanisms of Feiyangchangweiyan capsule (FYCWYC) on rat pelvic inflammatory disease (PID) model.

METHODS

To construct the rat PID model, upper genital tract was infected by multipathogen, and then drugs were orally administered for 8 days. The histological examination, immunohistochemical analysis, and ELISA were carried out. Furthermore, Western blotting was used to analyze the expression of Akt, MAPKs, NF-B p65, and IB- in uterus.

RESULTS

As the results showed, infiltrations of neutrophils and lymphocytes in uterus were significantly suppressed, and IL-1, IL-6, CXCL-1, and TNF- were also reduced in a dose-dependent manner. We also found that FYCWYC inhibited apoptosis induced by infection. Furthermore, FYCWYC could block the infection-induced nuclear translocation of NF-B. We found that FYCWYC treatment only decreased the phosphorylation of JNK induced by infection and had no effects on Akt and P38. Additional, the effects of SP600125, an inhibitor of phospho-JNK, were similar to the results of FYCWYC.

CONCLUSIONS

Taken together, our results demonstrated that FYCWYC had anti-inflammatory effect in pathogen-induced PID model, and the mechanism might be through inhibiting NF-B nuclear translocation which is mediated by JNK.

摘要

目的

在本研究中,我们旨在阐明飞扬肠胃炎胶囊(FYCWYC)对大鼠盆腔炎(PID)模型的预防作用及可能机制。

方法

构建大鼠PID模型,通过多种病原体感染上生殖道,然后口服给药8天。进行组织学检查、免疫组化分析和酶联免疫吸附测定(ELISA)。此外,采用蛋白质印迹法分析子宫中Akt、丝裂原活化蛋白激酶(MAPKs)、核因子-κB p65(NF-κB p65)和IκBα的表达。

结果

结果显示,子宫中中性粒细胞和淋巴细胞浸润明显受到抑制,白细胞介素-1(IL-1)、白细胞介素-6(IL-6)、CXC趋化因子配体-1(CXCL-1)和肿瘤坏死因子-α(TNF-α)也呈剂量依赖性降低。我们还发现FYCWYC抑制感染诱导的细胞凋亡。此外,FYCWYC可阻断感染诱导的NF-κB核转位。我们发现FYCWYC处理仅降低感染诱导的应激活化蛋白激酶(JNK)磷酸化,对Akt和p38无影响。另外,磷酸化JNK抑制剂SP600125的作用与FYCWYC的结果相似。

结论

综上所述,我们的结果表明FYCWYC在病原体诱导的PID模型中具有抗炎作用,其机制可能是通过抑制由JNK介导的NF-κB核转位。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aeeb/5851019/a4cf38886e96/ECAM2018-8476147.001.jpg

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