4.7 Article

Traditional Chinese Medicine prescription Huang-Qi-Jian-Zhong-Tang ameliorates indomethacin-induced duodenal ulcers in rats by affecting NF-ΚB and STAT signaling pathways

期刊

BIOMEDICINE & PHARMACOTHERAPY
卷 156, 期 -, 页码 -

出版社

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2022.113866

关键词

Traditional Chinese Medicine; HQJZT; Duodenal ulcer; Inflammation; STAT; NF-?B

资金

  1. National Natural Science Foundation of China
  2. Science and Technology Innovation Program of Hunan Province
  3. Science & Research Project of the Education Department of Hunan Province
  4. [81703920]
  5. [2021RC3101]
  6. [21A0240]

向作者/读者索取更多资源

This study investigated the protective effects of Huang-Qi-Jian-Zhong-Tang (HQJZT) against Indomethacin (IND)-induced duodenal ulceration in rats and the underlying mechanisms. The results showed that HQJZT effectively protected the duodenal mucosa by improving ulcer index, tissue architecture, and blood flow. Additionally, HQJZT regulated the expression of inflammation-related genes through NF-κB and STAT signaling pathways.
Huang-Qi-Jian-Zhong-Tang (HQJZT) is a well-known traditional Chinese herbal formulation. This study aimed to investigate the duodenoprotective properties of HQJZT against Indomethacin (IND)-induced duodenal ulceration in rats, and the mechanisms involved, particularly through NF-kappa B and STAT signaling pathways. Our results showed that HQJZT completely protected the duodenal mucosa from ulceration caused by IND, as indicated by improved macroscopic and histological appearances. There was a significant decrease in ulcer index and microscopic score, an increase in villus height and crypt depth, and a normalization of the tissue architecture of the duodenum in rats following HQJZT treatment. Blood flow into the duodenal mucosa was significantly increased after HQJZT administration. HQJZT significantly increased PGE2 and NO levels in the duodenal mu-cosa. A significant reduction in the production of pro-inflammatory cytokines IL-1 beta, IL-6, and TNF-alpha was observed in the duodenal mucosa under treatment with HQJZT. Mechanistically, the administration of HQJZT significantly lowered the duodenal protein expression of inflammation-related genes, including p-NF-kappa B and p-I kappa B beta, compared with the ulcer control group. Furthermore, the STAT signaling pathway-related protein markers p-JAK and p-STAT were significantly reduced in the HQJZT (1.30 and 2.60 g/kg) groups. As a result of these findings, HQJZT alleviates duodenal mucosal ulcers caused by IND. A protective effect of HQJZT on duodenal ulcers is attributed to its ability to improve mucosal blood flow, stimulate the production of cytoprotective mediators, minimize proinflammatory cytokines, and block the activation of NF-kappa B and STAT signaling pathways.

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