4.5 Article

Yan-Hou-Qing formula attenuates ammonia-induced acute pharyngitis in rats via inhibition of NF-κB and COX-2

期刊

出版社

BMC
DOI: 10.1186/s12906-020-03077-1

关键词

Pharyngitis; Inflammation; Yan Hou Qing; NF-kappa B; COX-2

资金

  1. Natural Science Foundation of China [81973915, 81773978]
  2. Guangdong Basic and Applied Basic Research Foundation [2019A1515010391, 2020A1515010592]
  3. Shenzhen Innovation of Science and Technology Commission [SZXK039, LGKCZSYS2019000046, JCYJ20170412103841386, 2017040320570626]

向作者/读者索取更多资源

Background: Yan Hou Qing (YHQ) is a Chinese medicinal formula designed to alleviate sore throat symptoms, but underlying mechanism of YHQ treatment for pharyngitis is poorly defined up to now. Methods: In this study, the modulation of YHQ on pharyngitis is investigated in ammonia-induced acute pharyngitis rat models. After treatment with YHQ or dexamethasone respectively for five consecutive days, all rats were sacrificed for biomolecular and histopathologic study. Protein expressions of MAPKs, NF-kappa B, COX-2 and 5-LOX in pharyngitis tissue were evaluated by western blot analysis and the levels of TNF-alpha, IL-6, prostaglandin (PG) E-2, leukotrienes (LT)-B(4)and LT-D(4)in pharyngeal tissue were measured via ELISA assay. Evans blue (EB) dye exudation test was performed parallelly to assess the integrity of pharyngeal tissue. Results: Compared with normal control group, EB dye exudation, and inflammatory cytokines in the model group were significantly increased, and the pharynx tissue was obviously infiltrated by inflammatory cells. YHQ treatment improved the inflammatory infiltrate in pharyngeal tissue, and reduced EB dye exudation in AP rat models. The up-regulated TNF-alpha and IL-6 in pharyngeal tissue of AP were significantly reduced by YHQ through inhibition of phosphorylation of p38, Erk and NF-kappa B. YHQ treatment also reversed the increased level of PGE(2)through down-regulation of COX-2. Conclusions: YHQ formula attenuated the pharyngitis related symptoms via suppression of COX-2 and phosphorylation of p38, Erk and NF-kappa B (p65).

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