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DIDS reduces ischemia/reperfusion-induced myocardial injury in rats.

AbstractBACKGROUND/AIMS:
Anion channels such as chloride channel are known to participate in the regulation of a wide variety of cellular processes including development, differentiation, proliferation, apoptosis and regeneration. This study was designed to examine the effect of the non-selective anion channel blocker 4,4'-Diisothiocyanostilbene-2, 2'-disulfonic acid (DIDS) on cardiac function and apoptosis using a rat model of ischemia/reperfusion (I/R).
METHODS:
Fifty male SD rats were randomly divided into the following groups including sham, I/R and I/R+DIDS (7, 14 or 28 mg/kg). In DIDS group, rats received DIDS treatment (4 ml/kg/hr) at the beginning of reperfusion for 2 hrs using a programmed micro-pump. Cardiac function was evaluated including left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP) as well as positive and negative maximal derivatives of left ventricular pressure (± dP/dt(max)). Myocardial infarct size was detected using the double staining with 2, 3, 5-triphenyl-2H-tetra-zolium chloride (TTC) and Evan's blue dye. DNA ladder, TUNEL assay, Bax and Bcl-2 protein levels were evaluated. Levels of ROS and Akt phosphorylation were detected.
RESULTS:
I/R injury compromised cardiac function as manifested by reduced LVSP and ± dP/dt(max) as well as pronounced apoptosis. I/R-induced cardiac anomalies were markedly ameliorated by DIDS. DIDS retarded I/R-induced myocardial infarct and apoptosis. In addition, DIDS ameliorated I/R-induced ROS production and Akt dephosphorylation in the heart.
CONCLUSION:
Taken together, our data revealed that DIDS may protect cardiomyocytes against I/R injury as evidenced by improved cardiac function, Bcl-2, Akt phosphorylation, and reduced myocardial apoptosis, Bax expression, ROS production and myocardial infarct size.
AuthorsXiaoming Wang, Yanan Cao, Mingzhi Shen, Bo Wang, Weiwei Zhang, Yan Liu, Xiaole He, Lin Wang, Yuesheng Xia, Mingge Ding, Xihui Xu, Jun Ren
JournalCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology (Cell Physiol Biochem) Vol. 35 Issue 2 Pg. 676-88 ( 2015) ISSN: 1421-9778 [Electronic] Germany
PMID25591913 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Copyright© 2015 S. Karger AG, Basel.
Chemical References
  • Chloride Channels
  • Reactive Oxygen Species
  • 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
Topics
  • 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid (administration & dosage, pharmacology)
  • Animals
  • Arterial Pressure (drug effects)
  • Chloride Channels
  • Gene Expression Regulation (drug effects)
  • Male
  • Myocardial Reperfusion Injury (drug therapy, metabolism, physiopathology)
  • Rats
  • Rats, Sprague-Dawley
  • Reactive Oxygen Species (metabolism)

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