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Abstract Title:

1,25(OH)Dalleviates oxidative stress and inflammation through up-regulating HMGCS2 in DSS-induced colitis.

Abstract Source:

Int Immunopharmacol. 2023 Dec ;125(Pt A):111131. Epub 2023 Oct 27. PMID: 38149572

Abstract Author(s):

Hong-Qian Wang, Meng-Xue Zhao, Shao-Cheng Hong, Xue He, Li Tao, Cheng-Cheng Tong, Jing Guan, De-Xiang Xu, Xi Chen

Article Affiliation:

Hong-Qian Wang

Abstract:

BACKGROUND: Previous study found that supplements with active vitamin D3 alleviated experimental colitis. The objective of this study was to investigate the possible role of 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2), a ketone synthase, on vitamin D3 protecting against experimental colitis.

METHODS: HMGCS2 and vitamin D receptor (VDR) were measured in UC patients. The effects of vitamin D deficiency (VDD) and exogenous 1,25(OH)Dsupplementation on experimental colitis were investigated in dextran sulfate sodium (DSS)-treated mice. DSS-induced oxidative stress and inflammation were analyzed in HT-29 cells. HMGCS2 was detected in 1,25(OH)D-pretreated HT-29 cells and mouse intestines. HMGCS2 was silenced to investigate the role of HMGCS2 in 1,25(OH)Dprotecting against experimental colitis.

RESULTS: Intestinal HMGCS2 downregulation was positively correlated with VDR reduction in UC patients. The in vivo experiments showed that VDD exacerbated DSS-induced colitis. By contrast, 1,25(OH)Dsupplementation ameliorated DSS-induced colon damage, oxidative stress and inflammation. HMGCS2 was up-regulated after 1,25(OH)Dsupplementation both in vivo and in vitro. Transfection with HMGCS2-siRNA inhibited antioxidant and anti-inflammatory effects of 1,25(OH)Din DSS-treated HT-29 cells.

CONCLUSION: 1,25(OH)Dsupplementation up-regulates HMGCS2, which is responsible for 1,25(OH)D-mediated protection against oxidative stress and inflammation in DSS-induced colitis. These findings provide a potential therapeutic strategy for alleviating colitis-associated oxidative stress and inflammation.

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