ArticleAnnals of translational medicine2022
EB1089 promotes the expression of vitamin D receptor in the intestinal epithelial cell line HT-29 and reduces lipopolysaccharide-induced inflammatory response.
Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Vitamins as modulators of neonatal intestinal injury.Frontiers in nutrition · 2026Review
- Vitamin D, immune microenvironment, and cervical lesions: mechanisms and therapeutic strategies from polyps to carcinoma.Frontiers in nutrition · 2025Review
- Lipopolysaccharide promotes apoptosis and oxidative injury of porcine small intestinal epithelial cells by down-regulating the expression of glutamine transporter ASCT2.Journal of animal science · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Background: EB1089 is a vitamin D receptor (VDR) agonist that reduces the inflammatory response. The specific pathway through which the inflammatory response is reduced is unclear, and this study is intended to investigate its effect on the inflammatory response through an LPS (lipopolysaccharide)-induced inflammation model of the intestinal epithelial cell line HT-29. Methods: We divided HT-29 cells into a control group, LPS group, and LPS + EB1089 group. Cell proliferation was detected with a Cell Counting Kit-8 (CCK-8) kit, and the apoptosis rate was determined through flow cytometry, the lactate dehydrogenase (LDH), interleukin-18 (IL-18), and interleukin-1β (IL-1β) contents were measured with enzyme-linked immunosorbent assay (ELISA), and the expression levels of ASC, Caspase-1, NLRP3, VDR, TLR4, MYD88, NF-κB and other proteins in the cells were detected by western blot. Results: Pretreatment with EB1089 pretreatment reduced the LPS-induced apoptosis of HT-29 cells. LDH content was evidently lower in the LPS + EB1089 group than in the LPS group. The LDH content in the LPS + EB1089 group was evidently lower than that in the LPS group. The protein expression levels of ASC, Caspase-1, NLRP3, TLR4, MyD88, and NF-κB in the LPS group were evidently increased compared with those in the control group; however, the protein expression of VDR evidently decreased. The protein expression levels of Caspase-1, NLRP3, TLR4, MyD88, and NF-κB in the LPS + EB1089 group were evidently lower than those in the LPS group; however, the VDR protein expression evidently increased in the LPS + EB1089 group. Conclusions: EB1089 promoted the VDR expression and reduced the LPS induced inflammation in HT-29 cells.
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Registered trials
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