Evidence-based complementary and alternative medicine : eCAM · 2018
Anti-Inflammatory Effect of Feiyangchangweiyan Capsule on Rat Pelvic Inflammatory Disease through JNK/NF-κB Pathway.
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Li Yao, Liu Yang, Yang Qian, Shi Zhihui, Xie Yanhua, Wang Siwang
Аннотация
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.
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.