title: Cholecalciterol cholesterol emulsion ameliorates experimental colitis via down-regulating the pyroptosis signaling pathway.
abstract: The therapeutic effect of 1,25(OH)2 vitamin D3 and its analog (paricalcitol) on experimental colitis in animals has been heavily demonstrated. However, the response to Cholecalciterol Cholesterol Emulsion (CCE), a precursor of 1,25(OH)2 vitamin D3, has not yet been reported. Whether pyroptosis is involved in colitic deterioration also remains unclear. Therefore, we adopted molecular biology and histology approaches to examine mechanisms by which CCE was able to regulate experimental colitis in the animal model induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS). Our data revealed that mice displayed a remarkable reduction in colonic histological scores, colonic inflammation and colonic histological damage. In addition, there was an overall improvement in general status (change in body weight, food and water intake, mental status, activity) and a 30% increase in survival rate due to the downregulation of pyroptosis following treatment with CCE. In conclusion, our data have provided evidence that CCE can attenuate the damage of experimental colitis by suppressing pyroptosis signaling.
authors.affiliation: Department of Clinical Nutrition, Shengjing Hospital of China Medical University, Shenyang 110004, China.
authors.forename: Yangyang
authors.initials: Y
authors.lastname: Xiong
authors.affiliation: School of Fundamental Sciences, China Medical University, Shenyang 110122, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Lou
authors.affiliation: Department of Clinical Nutrition, Shengjing Hospital of China Medical University, Shenyang 110004, China.
authors.forename: Han
authors.initials: H
authors.lastname: Su
authors.affiliation: Department of Clinical Nutrition, Shengjing Hospital of China Medical University, Shenyang 110004, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Fu
authors.affiliation: Department of Clinical Nutrition, Shengjing Hospital of China Medical University, Shenyang 110004, China. Electronic address: kongj1@sj-hospital.org.
authors.forename: Juan
authors.initials: J
authors.lastname: Kong
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002117:Calcitriol / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D002118:Calcium / Q000097:blood; D020170:Caspase 1 / Q000235:genetics / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D002762:Cholecalciferol / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D002784:Cholesterol / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D003092:Colitis / Q000139:chemically induced / Q000401:mortality / Q000517:prevention & control*; D003106:Colon / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D004655:Emulsions; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D020382:Interleukin-18 / Q000235:genetics / Q000378:metabolism; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D008297:Male; D008807:Mice, Inbred BALB C; D010758:Phosphorus / Q000097:blood; D000069292:Pyroptosis / Q000187:drug effects*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects*; D015996:Survival Rate; D014302:Trinitrobenzenesulfonic Acid; D014808:Vitamin D Deficiency / Q000097:blood / Q000188:drug therapy; D014815:Vitamins / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D004655:Emulsions; D020382:Interleukin-18; D053583:Interleukin-1beta; D014815:Vitamins; D002762:Cholecalciferol; D010758:Phosphorus; D014302:Trinitrobenzenesulfonic Acid; D002784:Cholesterol; D020170:Caspase 1; D002117:Calcitriol; D002118:Calcium
keywords: CCE; IBD; Pyroptosis; TNBS; VDR