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Evidence-Based Complementary and Alternative Medicine
Volume 2018, Article ID 8476147, 10 pages
Research Article

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

1School of Pharmacy, Shaanxi University of Chinese Medicine, Xianyang 712000, China
2College of Chemistry and Pharmacy, Northwest Agriculture and Forestry University, Yangling 712100, China
3Department of Natural Medicine, School of Pharmacy, The Fourth Military Medical University, Xi’an 710032, China
4Shaanxi Junbisha Pharmaceutical Limited Company, Shaanxi, China

Correspondence should be addressed to Yanhua Xie; nc.ude.ummf@hnayeix and Siwang Wang; nc.ude.ummf@wisgnaw

Received 8 November 2017; Revised 22 January 2018; Accepted 24 January 2018; Published 28 February 2018

Academic Editor: Kuzhuvelil B. Harikumar

Copyright © 2018 Yao Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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-κB p65, and IκB-α in uterus. Results. As the results showed, infiltrations of neutrophils and lymphocytes in uterus were significantly suppressed, and IL-1β, IL-6, CXCL-1, and TNF-α 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-κB. 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-κB nuclear translocation which is mediated by JNK.