Corynoline ameliorates dextran sulfate sodium-induced colitis in mice by modulating Nrf2/NF-κB pathway

  • Immunopharmacol Immunotoxicol. 2022 Aug 18;1-9. doi: 10.1080/08923973.2022.2112218.
Haihua Zhang  1 ,  Wuying Lang  2 ,  Sufen Li  1 ,  Chao Xu  3 ,  Xiumin Wang  4 ,  Yunyu Li  1 ,  Zhiqiang Zhang  1 ,  Tonglei Wu  1 ,  Minshan Feng  1
Affiliations
  • 1. Hebei Key Laboratory of Specialty Animal Germplasm Resources Exploration and Innovation, Hebei Normal University of Science and Technology, Qinhuangdao, Hebei, People's Republic of China.
  • 2. College of Biology Pharmacy and Food Engineering, Shangluo University, Shangluo, Shaanxi, People's Republic of China.
  • 3. Institute of Special Animal and Plant Sciences, Chinese Academy of Agricultural Sciences, Changchun, Jilin, People's Republic of China.
  • 4. Beijing Centre Technology Co., Ltd., Beijing, People's Republic of China.
PMID: 35980837 DOI: 10.1080/08923973.2022.2112218
Abstract

Objective: Corynoline is an active substance extracted from Corydalis bungeana Turcz and exerts a therapeutic effect in multiple diseases by alleviating inflammatory response. The present study sought to elucidate the role of corynoline in ulcerative colitis (UC).

Methods: The experimental colitis models were induced in BALB/c mice via receiving a drinking water supplemented with 3.5% (I) dextran sulfate sodium (DSS) ad libitum for 7 days.

Results: Corynoline administration inhibited body weight loss, colon shortening, disease activity index and colonic pathomorphological changes in DSS-treated mice. Besides, corynoline down-regulated the levels of pro-inflammatory interleukin (IL)-1β, IL-6 and tumor necrosis factor Alpha (TNF-α), as well as decreased myeloperoxidase (MPO) activity in the colon of DSS-treated mice. In addition, severe oxidative stress in the colonic tissues of DSS-treated was mitigated by corynoline treatment. However, these beneficial effects were reversed by a specific nuclear factor E2-related factor 2 (Nrf2) inhibitor ML385 intervention. Further evidence confirmed that corynoline promoted Nrf2 nuclear migration and heme oxygenase-1 gene expression in the colonic tissues of UC mice. Besides, corynoline treatment restrained colonic nuclear factor-kappa B (NF-κB) activation as proved by the decrease in phosphorylation and nuclear translocation of NF-κB.

Conclusions: Corynoline ameliorates DSS-induced mouse colitis, which may provide a promising therapeutic strategy for UC treatment.

Keywords
Nrf2/NF-κB pathway; Ulcerative colitis; corynoline; inflammation; oxidative stress.
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