Zongming Shi1, Hui Ye1, Jing Yu1, Xuezhi Zhang1, Hong Cheng2, Jiang Li2. 1. Department of Integrated Traditional Chinese Medicine, Peking University First Hospital, Beijing 100034, China. 2. Department of Gastroenterology, Peking University First Hospital, Beijing 100034, China.
Abstract
OBJECTIVE: To investigate the inhibitory effect of Jinghua Weikang capsule (JWC) on gastric inflammation induced by Helicobacter pylori (H. pylori) via the nuclear factor-kappa B (NF-¦ÊB) signaling pathway in Kunming mice. METHODS: We investigated the anti-inflammation potential of JWC extract in vivo in a H. pylori-induced gastritis mouse model. The expression of inflammation-related molecules was evaluated by Western blotting, and the concentrations of in vivo inflammatory markers were measured by enzyme-linked immunosorbent assay. Inflammatory cell infiltration was evaluated by histopathological examination, and mRNA levels of related genes were evaluated by quantitative reverse transcription polymerase chain reaction. RESULTS: JWC had a dose-dependent protective effect against H. pylori-induced gastritis by protecting gastric epithelial cells and inhibiting inflammatory cell infiltration. Mechanistically, JWC decreased the protein levels of phosphorylated I¦ÊB¦Á and NF-¦ÊB p65, mRNA levels of NF-¦ÊB pathway molecules, and plasma levels of tumor necrosis factor-¦Á and interleukin 1 beta. CONCLUSION: An important finding of our study is that JWC attenuated gastrointestinal inflammation and ulceration and exerted a protective effect against gastric injury via inhibition of inflammation reactions and regulating the canonical NF-κB signaling pathway in vivo.
OBJECTIVE: To investigate the inhibitory effect of Jinghua Weikang capsule (JWC) on gastric inflammation induced by Helicobacter pylori (H. pylori) via the nuclear factor-kappa B (NF-¦ÊB) signaling pathway in Kunming mice. METHODS: We investigated the anti-inflammation potential of JWC extract in vivo in a H. pylori-induced gastritismouse model. The expression of inflammation-related molecules was evaluated by Western blotting, and the concentrations of in vivo inflammatory markers were measured by enzyme-linked immunosorbent assay. Inflammatory cell infiltration was evaluated by histopathological examination, and mRNA levels of related genes were evaluated by quantitative reverse transcription polymerase chain reaction. RESULTS: JWC had a dose-dependent protective effect against H. pylori-induced gastritis by protecting gastric epithelial cells and inhibiting inflammatory cell infiltration. Mechanistically, JWC decreased the protein levels of phosphorylated I¦ÊB¦Á and NF-¦ÊB p65, mRNA levels of NF-¦ÊB pathway molecules, and plasma levels of tumor necrosis factor-¦Á and interleukin 1 beta. CONCLUSION: An important finding of our study is that JWC attenuated gastrointestinal inflammation and ulceration and exerted a protective effect against gastric injury via inhibition of inflammation reactions and regulating the canonical NF-κB signaling pathway in vivo.
Entities:
Keywords:
Helicobacter pylori; Jinghua Weikang capsule; NF-kappa B; Signal transduction