Premium
The influence of the Chuyou Yuyang granule on the Toll‐like receptor/nuclear factor‐κB signal pathway in Helicobacter pylori ‐positive peptic ulcer patients
Author(s) -
Yang Fang,
Ge Guiping,
Shen Wen,
Chen Liang
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28647
Subject(s) - helicobacter pylori , medicine , tlr4 , tumor necrosis factor alpha , proinflammatory cytokine , cytokine , western blot , h&e stain , interleukin 6 , toll like receptor , inflammation , gastroenterology , receptor , immunohistochemistry , biology , gene , innate immune system , biochemistry
Background The cure rate of Helicobacter pylori (HP)‐positive peptic ulcer has appeared to downward trend, and the resistance of the ulcer relapse has become a hot issue. Methods Hematoxylin and eosin staining was used to detect the repair of the damaged tissues in patients after treatment with the Chuyou Yuyang granule (CYYY). Elisa was used to analyze the expression of cytokine interleukin 18 (IL‐18) and tumor necrosis factor α (TNF‐α) in the patients' serum. Western blot analysis was used to explore the mechanism of the CYYY. Reverse‐transcription polymerase chain reaction (RT‐PCR) was used to detect the expression of microRNA‐155a (miR‐155a) and miR‐146a in the blood of the patients and to confirm whether CYYY could cure peptic ulcer through regulation of miR‐155a and miR‐146a. Results The damaged gastric mucosal tissues of ulcer patients were significantly repaired by treating with CYYY. The pro‐inflammatory cytokine IL18 and TNF‐α were notably repressed after treating with CYYY. In addition, CYYY played a key role in regulation of the Toll‐like receptor (TLR4)/nuclear factor‐κB (NF‐κB) signal pathway and the expression of miR‐155a and miR‐146a. Conclusion CYYY was a highly effective therapeutic method for peptic ulcer patients by inhibiting the activation of the TLR4/NF‐κB signal pathway and suppressing the expression of miR‐155a and miR‐146a.