Dioscin ameliorates intestinal ischemia/reperfusion injury via adjusting miR-351-5p/MAPK13-mediated inflammation and apoptosis. (January 2019)

• Record Type: Journal Article
• Authors: Zheng, Lingli; Han, Xu; Hu, Yupeng; Zhao, Xuerong; Yin, Lianhong; Xu, Lina; Qi, Yan; Xu, Youwei; Han, Xu; Liu, Kexin; Peng, Jinyong
• Is Part Of: Pharmacological research. Volume 139(2019)
• Page Start: 431
• Page End: 439
• Publication Date: 2019-01
• Subjects: II/R intestinal ischemia-reperfusion -- H/R hypoxia-reoxygenation -- IPC ischemia-reperfusion precondition -- IPO ischemia-reperfusion post-conditioning -- FBS fetal bovine serum -- NC negative control -- SMA superior mesenteric artery -- MAPK13 mitogen-activated protein kinase 13 -- PKD1 protein kinase D1 -- p-PKD1 phosphor- protein kinase D1 -- NF-κB nuclear factor kappa B -- Cytc cytochrome c -- Apaf-1 apoptotic protease activating factor-1 -- HE hematoxylin-eosin -- TCMs traditional Chinese medicines -- TUNEL TdT-mediated dUTP Nick-End Labeling -- IL-1β interleukin 1 beta -- IL-6 interleukin 6 -- TNF-α tumor necrosis factor alpha -- ICAM-1 intercellular cell adhesion molecule-1; Apoptosis -- Dioscin -- Inflammation -- Intestinal ischemia/reperfusion -- miR- 351-5p -- MAPK13; Pharmacology -- Periodicals; Pharmacology -- Periodicals; Research -- Periodicals; Médicaments -- Recherche -- Périodiques; Pharmacologie -- Périodiques; 615.105
• DOI: 10.1016/j.phrs.2018.11.040
• Languages: English
• ISSNs: 1043-6618

Abstract

Graphical abstract: Abstract: Inflammatory reaction and cell apoptosis are two important processes in intestinal ischemia/reperfusion (II/R) injury, and exploration of effective lead compounds against II/R injury via regulating inflammation and apoptosis is critical important. In this paper, the results indicated that dioscin significantly increased cell viability, and inhibited inflammation and apoptosis caused by hypoxia-reoxygenation (H/R) injury in IEC-6 cells. in vivo II/R injury, dioscin markedly suppressed inflamma- tion and apoptosis, improved pathological changes, and depressed chiu' score in rats. Mechanistic studies indicated that dioscin notably up-regulated the expression level of MAPK13 through decreasing miR-351-5p level, and thereby decreased the expression levels of p-PKD1, NF-κB, Apaf-1, cleaved Caspase-3 and cleaved Caspase-9. Furthermore, miR-351-5p mimic and inhibitor experiments in IEC-6 cells further proved that dioscin up-regulated MAPK13 expression by decreasing miR-351-5p level to inhibit inflammation and apoptosis. Therefore, dioscin showed protective effect against II/R injury via adjusting miR-351-5/MAPK13-mediated inflammation and apoptosis. Dioscin should be considered as one potent candidate and miR-351-5/ MAPK13 should be one effective drug target for the treatment of II/R injury.