Toxicology and applied pharmacology · 2024
Fucoxanthin ameliorates ulcerative colitis by maintaining the epithelial barrier via blocking JAK2/STAT3 signaling pathway.
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Ma Jingjing, Yue Simei, Liu Yinghui, Gong Lingjiao, He Pengzhan, Yang Yingjie, Fu Zhengxin, Han Danxiang, Hu Qiang, Liao Fei, Xu Lin
Аннотация
BACKGROUND: The clinical efficacies of Ulcerative colitis (UC) are far from satisfactory. Fucoxanthin (FUC) is a marine carotenoid that is abundant in seaweed and microalgae. It has been reported that FUC can possess anti-inflammatory and antioxidant. However, its mechanism and role in UC is yet to be clarified. This study aimed to investigate the protective effect and potential mechanism of FUC extracted from the diatom Phaeodactylum tricornutm on dextran sodium sulfate (DSS) -induced colitis.
METHODS: Animal UC model was induced by DSS and cellular model was established by TNF-α. Immunohistochemical staining, Western blot, RT-qPCR, and immunofluorescence were used to assess the inflammatory responses and epithelial barrier in vivo and in vitro models.
RESULTS: The results showed that FUC attenuates DSS-induced colitis by ameliorating the epithelial mucosal barrier. Moreover, FUC possessed antioxidant and anti-inflammatory effects on NCM460 cells. JAK/STAT activator RO8191 could reverse these changes.
CONCLUSION: FUC exerted anti-inflammatory and antioxidant effects via the JAK2/STAT3 signaling pathway, and served as a potential therapeutic agent for the treatment of UC.
METHODS: Animal UC model was induced by DSS and cellular model was established by TNF-α. Immunohistochemical staining, Western blot, RT-qPCR, and immunofluorescence were used to assess the inflammatory responses and epithelial barrier in vivo and in vitro models.
RESULTS: The results showed that FUC attenuates DSS-induced colitis by ameliorating the epithelial mucosal barrier. Moreover, FUC possessed antioxidant and anti-inflammatory effects on NCM460 cells. JAK/STAT activator RO8191 could reverse these changes.
CONCLUSION: FUC exerted anti-inflammatory and antioxidant effects via the JAK2/STAT3 signaling pathway, and served as a potential therapeutic agent for the treatment of UC.