Dexmedetomidine inhibits pyroptosis by down-regulating miR-29b in myocardial ischemia reperfusion injury in rats.

International Immunopharmacology
Yi ZhongHong Gao

Abstract

Dexmedetomidine (DEX) was reported to protect heart against ischemic-reperfusion (IR) but the mechanism herein remains elusive. This study aims to explore the mechanism of DEX on pyroptosis induced by myocardial ischemic reperfusion (MIR). MIR rat models were established and injected DEX or miR-29b agomir/antagomir separately. The possible effect of DEX or miR-29b on myocardial cells was assessed according to measurement on creatine kinase-MB (CK-MB), cardiac troponin I (cTnI), interleukin-1β (IL-1β) and interleukin-18 (IL-18), myocardial infarction size, myocardial injury and apoptosis. Western blot determined the expression levels of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), apoptosis-associated speck-like protein containing CARD (ASC) and cleaved-caspase-1. Hypoxia/reoxygenation (H/R) cell model was established. The lactate dehydrogenase (LDH) content released by myocardial cells was examined. The relation between miR-29b and FoxO3a was confirmed by dual luciferase reporter gene assay. FoxO3a or ARC level was elevated in H/R myocardial cells to detect its effect on pyroptosis. MIR rat models were successfully established, in which cell pyroptosis was triggered as evidenced by increased expres...Continue Reading

References

Jul 21, 2010·The American Journal of Cardiology·Aslan T Turer, Joseph A Hill
Jan 3, 2013·The Journal of Clinical Investigation·Derek J Hausenloy, Derek M Yellon
May 2, 2013·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·Savita KhannaChandan K Sen
Jul 2, 2015·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·Yang WangGuo-Yuan Yang
Oct 23, 2015·Mediators of Inflammation·Seahyoung LeeKi-Chul Hwang
Nov 27, 2015·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·Jaime A RiquelmeSergio Lavandero
Dec 23, 2016·Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology·Haoyu WuZhen Dong
Sep 6, 2017·Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology·Qiuyue ZhangHongyu Liu
Sep 1, 2018·American Journal of Physiology. Heart and Circulatory Physiology·Stefano ToldoAntonio Abbate
Dec 14, 2018·Cell Proliferation·Zeng ZhaolinWang Zuo
Mar 25, 2019·Journal of Clinical Medicine·Sebastian BunteRagnar Huhn
Apr 10, 2019·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Liang HeJinqiao Qian
Apr 27, 2019·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Juan YuJinqiao Qian
Jun 1, 2019·Journal of Molecular and Cellular Cardiology·Zixin ChenYaoliang Tang
Jul 25, 2019·International Journal of Biological Sciences·Cheng ZengHongmei Tan
Jul 30, 2019·Frontiers in Immunology·Thiago Henrique Caldeira de OliveiraFlávio Almeida Amaral
Aug 1, 2019·Physiological Reviews·Dominic P Del ReRichard N Kitsis
Aug 17, 2019·American Journal of Physiology. Heart and Circulatory Physiology·Paras K MishraTakashi Matsui

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis