期刊
CHINESE MEDICINE
卷 17, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s13020-022-00599-3
关键词
Anemonin; Acute ulcerative colitis; Inflammation; PKC-theta
资金
- Shandong Traditional Chinese Medicine Science and Technology Development Plan [2017056]
- Jinan Clinical Medical Science and Technology Innovation Plan [202019154]
The study found that anemonin can improve body weight loss, shortened colon length, increased DAI, and induced pathological changes in the colon tissue of UC mice. Anemonin inhibits DSS-induced colon tissue inflammation and also attenuates LPS-induced cytokine production in HT-29 cells. The anti-inflammatory effects of anemonin may be mediated through targeting PKC-theta.
Background: Ulcerative colitis (UC) is an inflammatory bowel disease that causes continuous mucosal inflammation. Anemonin is a natural molecule from the Ranunculaceae and Gramineae plants that exerts anti-inflammatory properties. This study aimed to explore the effects and mechanisms of anemonin on UC. Methods: C57BL/6 mice were administered dextran sulphate sodium (DSS; 3% [w/v]) to establish an animal model of UC. Mice were treated with an intraperitoneal injection of anemonin. Body weight and the disease activity index (DAI) were recorded. Haematoxylin and eosin staining, RT-qPCR, ELISA, and western blotting were performed to evaluate the histopathological changes and tissue inflammation. HT-29 cells were treated with lipopolysaccharide (LPS) and anemonin. Cell inflammation was evaluated using RT-qPCR and western blotting. The target proteins of anemonin were predicted using bioinformatics analysis and confirmed in vitro and in vivo. Results: Anemonin improved DSS-induced body weight loss, shortened colon length, increased DAI, and induced pathological changes in the colon tissue of mice. Anemonin inhibited DSS-induced colon tissue inflammation as the release of IL-1 beta, INF-alpha, and IL-6 was significantly suppressed. Additionally, anemonin attenuated LPS-induced cytokine production in HT-29 cells. PKC-theta was predicted as a target protein of anemonin. Anemonin did not affect PRKCQ gene transcription, but inhibited its translation. PRKCQ overexpression partially reversed the protective effects of anemonin on HT-29 cells. Adeno-associated virus delivery of the PRKCQ vector significantly reversed the protective effects of anemonin on the mouse colon. Conclusions: Anemonin has the potential to treat UC. The anti-inflammatory effects of anemonin may be mediated through targeting PKC-theta.
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