ArticleMedical science monitor : international medical journal of experimental and clinical research2017
1,25(OH)2D3 Protects Liver Fibrosis Through Decreasing the Generation of TH17 Cells.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Calcitriol attenuates liver fibrosis through hepatitis C virus nonstructural protein 3-transactivated protein 1-mediated TGF β1/Smad3 and NF-κB signaling pathways.World journal of gastroenterology · 2023Article
- Calcipotriol attenuates liver fibrosis through the inhibition of vitamin D receptor-mediated NF-κB signaling pathway.Bioengineered · 2022Article
- The role of interleukin-17 in the pathogenesis of systemic sclerosis: Pro-fibrotic or anti-fibrotic?Journal of scleroderma and related disorders · 2021Review
- 17,20S(OH)International journal of molecular sciences · 2021Article
- Novel Immune Subsets and Related Cytokines: Emerging Players in the Progression of Liver Fibrosis.Frontiers in medicine · 2021Review
- Article
- Serum vitamin D status in sick cats with and without cholestatic liver disease.Journal of feline medicine and surgery · 2020Article
- 1,25(OH)Cell cycle (Georgetown, Tex.) · 2019Article
- 1,25-Dihydroxyvitamin D3 Prevents Epithelial-Mesenchymal Transition of HMrSV5 Human Peritoneal Mesothelial Cells by Inhibiting Histone Deacetylase 3 (HDAC3) and Increasing Vitamin D Receptor (VDR) Expression Through the Wnt/β-Catenin Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Interleukin-17 pathways in systemic sclerosis-associated fibrosis.Rheumatology international · 2019Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The aim of this study was to study the effects of 1-alpha,25-dihydroxy-cholecalcifero (1,25(OH)2D3) on liver fibrosis and the generation of Th17 cells in vivo and in vitro. MATERIAL AND METHODS Thirty C57 mice were randomly divided into control, model, and treatment groups. Hepatic fibrosis was induced by subcutaneous injection of CCl4. Liver fibrosis condition was evaluated through pathological inspection and blood biochemical examination of liver function. Immunohistochemical assays were used to detect the expression of α-SMA, TGF-β, and collagen I to observe hepatic stellate cell activation level. Flow cytometry, ELISA, and RT-PCR were performed to explore the association between 1,25(OH)2D3 and Th17 cell differentiation. RESULTS Collagen I, TGF-β, and α-SMA were decreased after 1,25(OH)2D3 treatment. Consistently, RORγt mRNA and the rate of Th17 cells was significantly reduced after 1,25(OH)2D3 treatment. In vitro, the proportion of Th17 cells was also obviously reduced in the 1,25(OH)2D3 group, and mRNA levels of IL-17A, IL-22, RORγt, and RORa were significantly decrease in the 1,25(OH)2D3 group compared to the control group. CONCLUSIONS Treatment with 1,25(OH)2D3 can alleviate the damage caused by liver fibrosis. Experiments in vivo and in vitro showed that 1,25(OH)2D3 treatment deceased the rates of Th1 and Th17 cells and increased the rate of Th2 cells. The level of IL-17A, IL-22 and IFN-γ were decreased, while the level of IL-4 was increased by the treatment of 1,25(OH)2D3.
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