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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >The Anti-Inflammatory Effect of Feiyangchangweiyan Capsule and Its Main Components on Pelvic Inflammatory Disease in Rats via the Regulation of the NF-κB and BAX/BCL-2 Pathway
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The Anti-Inflammatory Effect of Feiyangchangweiyan Capsule and Its Main Components on Pelvic Inflammatory Disease in Rats via the Regulation of the NF-κB and BAX/BCL-2 Pathway

机译:Feiyangchangweiyyan胶囊及其主要成分对大鼠NF-κB和BCCL-2途径大鼠盆腔炎疾病的抗炎作用

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摘要

Although gastroenteritis and pelvic inflammatory disease (PID) occur in the gastrointestinal tract and pelvis, respectively, they display similar pathogeneses. The incidence of inflammation in these conditions is usually associated with dysbacteriosis, and, at times, they are caused by the same pathogenic bacteria, Escherichia coli and Streptococcus aureus. Feiyangchangweiyan capsule (FYC) is a traditional Chinese patent medicine that is widely used to treat bacterial dysentery and acute and chronic gastroenteritis. However, whether it has an effect on PID is unclear. The aim of this study was to investigate the anti-inflammatory effect of FYC and its main components, gallic acid (GA), ellagic acid (EA), and syringin (SY), on a pathogen-induced PID model and illustrate their potential mechanism of action. Female specific pathogen-free SD rats (n = 1110) were randomly divided into control, PID, FYC, GA, EA, SY, GA + EA, GA + SY, EA + SY, GA + EA + SY, and Fuke Qianjin capsule (FKC) positive groups. Histological examination and enzyme-linked immunosorbent assay (ELISA) were carried out as well as western blot analysis to detect the expression of NF-κB, BAX, BCL-2, and JNK. In this study, FYC and its main components dramatically suppressed the infiltration of inflammatory cells, reduced the production of IL-1β, TNF-α, and MCP-1, and elevated the IL-10 level to varying degrees. We also found that FYC and its main components inhibited the expression of BAX induced by infection and increased the expression of Bcl-2. FYC, GA, EA, and SY could also block the activation of the NF-κB pathway. Finally, we found that the phosphorylation of JNK could be decreased by FYC, GA, and SY. FYC and its main components exhibit anti-inflammatory effect on a pathogen-induced PID model by regulating the NF-κB and apoptosis signaling pathways.
机译:尽管胃肠炎和盆腔炎(PID)分别发生在胃肠道和骨盆中,但它们显示出类似的病原体。这些条件下炎症的发病率通常与缺血剂相关,并且有时它们是由同一致病菌,大肠杆菌和链球菌的金黄色葡萄球菌引起的。 Feiyangchangweiyan胶囊(FYC)是一种传统的中国专利药,广泛用于治疗细菌痢疾和急性和慢性胃肠炎。但是,它是否对PID有效尚不清楚。本研究的目的是探讨FYC及其主要成分,无碱酸(GA),鞣酸(EA)和切割蛋白(SY)对病原体诱导的PID模型的抗炎作用,并说明其潜在机制行动。将雌性特异性病原体SD大鼠(n = 1110)随机分为对照,PID,FYC,GA,EA,SY,GA + EA,GA + SY,EA + SY,GA + EA + SY,以及FUKE Qianjin胶囊(FKC)阳性群体。进行组织学检查和酶联免疫吸附测定(ELISA)以及Western印迹分析,以检测NF-κB,BAX,BCL-2和JNK的表达。在本研究中,FYC及其主要成分显着抑制了炎性细胞的渗透,降低了IL-1β,TNF-α和MCP-1的产生,并将IL-10水平升高到不同程度。我们还发现FYC及其主要成分抑制了感染诱导的BAX的表达,并增加了BCL-2的表达。 FYC,GA,EA和SY也可能阻断NF-κB途径的激活。最后,我们发现JNK的磷酸化可以通过FYC,GA和SY减少。 FYC及其主要成分通过调节NF-κB和凋亡信号通路对病原体诱导的PID模型表现出抗炎作用。

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