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An Ethanolic Extract of Allium hookeri Root Alleviates Reflux Esophagitis and Modulates NF-κB Signaling

Reflux esophagitis (RE) is a kind of gastroesophageal reflux disease, of which an esophageal inflammatory lesion is caused by the contents of the stomach and duodenum flowing back into the esophagus. Allium hookeri is a plant possessing both nutritional and medicinal properties. In our study, we inv...

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Detalles Bibliográficos
Autores principales: Nan, Li, Nam, Hyeon Hwa, Choo, Byung Kil, Park, Jin Cheon, Kim, Dae Geun, Lee, Jeong Ho, Moon, Kwang Hyun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6196785/
https://www.ncbi.nlm.nih.gov/pubmed/30402117
http://dx.doi.org/10.1155/2018/1834681
Descripción
Sumario:Reflux esophagitis (RE) is a kind of gastroesophageal reflux disease, of which an esophageal inflammatory lesion is caused by the contents of the stomach and duodenum flowing back into the esophagus. Allium hookeri is a plant possessing both nutritional and medicinal properties. In our study, we investigated the inhibition effect of inflammation of A. hookeri root extract (AHE) on inflammatory RAW264.7 macrophage cells induced by lipopolysaccharide and rat models of RE. The results showed that AHE significantly reduced the production of nitric oxide (NO) and the protein expression levels of various mediators related to inflammation including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and inflammatory cytokines such as interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α). Furthermore, AHE also inhibited the nuclear translocation of nuclear factor kappa B (NF-κB) by inhibiting the phosphorylation IκBα. In addition, AHE administration significantly ameliorated esophageal mucosal damage upon histological evaluation of RE in rats. AHE was also found to downregulate the expression levels of proteins such as COX-2, TNF-α, and IL-1β in the rat esophagus. AHE markedly attenuated activation of NF-κB and phosphorylation of IκBα at the same time. These results indicated that AHE suppressed LPS-induced inflammatory responses in RAW264.7 cells and may help reduce the development of esophagitis through the modulation of inflammation by regulating NF-κB activation.