Liuwei Anxiao San protects gastric mucosa from gastric ulcer in rats by regulating the JAK2/STAT3 pathway

  • Tissue Cell. 2023 Aug:83:102145. doi: 10.1016/j.tice.2023.102145.
Ze Qu  1 ,  Dong Jiang  2 ,  Yan Liu  3 ,  Mingxing Hou  4
Affiliations
  • 1. Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210029, China; Geriatrics Center, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010050, China.
  • 2. Hand and Foot Microscopy Center, the Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010050, China.
  • 3. Department of Medical Administration, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010050, China.
  • 4. Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210029, China; Department of Gastrointestinal Surgery, Affiliated Hospital of Inner Mongolia Medical University, No. 5, Xinhua West Street, Huimin District, Hohhot, Inner Mongolia 010050, China. Electronic address: [email protected].
PMID: 37437331 DOI: 10.1016/j.tice.2023.102145
Abstract

Mongolian medicine prescriptions are recognized as promising gastroprotective agents. This study is to explore the effects and mechanisms of Liuwei Anxiao San (LAS) in gastric ulcer (GU). GU rat models were established using acetic acid, followed by treatment with LAS at different doses and/or the JAK2 agonist Coumermycin A1 (CA1). The ulcerous area and inhibition rates were calculated. The mucosal damage and cell Apoptosis in gastric tissues were assessed by H&E and TUNEL staining. The activities of SOD, GSH-Px, and CAT, and MDA levels were measured. The levels of pro-inflammatory and anti-inflammatory factors were determined by ELISA. The activation of the JAK2/STAT3 pathway was determined by Western blot. As the results suggested, LAS dose-dependently ameliorated gastric mucosal damage and inhibited oxidative stress and inflammatory response, evidenced by increased activities of SOD, GSH-Px, and CAT, decreased MDA level, increment of anti-inflammatory factors and decrement of pro-inflammatory factors, and inhibited the activation of the JAK2/STAT3 pathway in GU rats. CA1 partly abolished the function of LAS on gastric mucosal injury, oxidative stress, and inflammation in GU rats. In conclusion, LAS protects against gastric mucosal injury in GU rats through inhibition of oxidative stress and inflammation by suppressing the JAK2/STAT3 pathway.

Keywords
Coumermycin A1; Gastric ulcer; Inflammation; JAK2/STAT3 pathway; Liuwei Anxiao San; Oxidative stress.
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