Details

Autor(en) / Beteiligte

• Wang, Xiaoming
• Cao, Yanan
• Shen, Mingzhi
• Wang, Bo
• Zhang, Weiwei
• Liu, Yan
• He, Xiaole
• Wang, Lin
• Xia, Yuesheng
• Ding, Mingge
• Xu, Xihui
• Ren, Jun

Titel

DIDS Reduces Ischemia/Reperfusion-Induced Myocardial Injury in Rats

Ist Teil von

• Cellular physiology and biochemistry, 2015-01, Vol.35 (2), p.676-688

Ort / Verlag

Basel, Switzerland: Cell Physiol Biochem Press GmbH & Co KG

Erscheinungsjahr

2015

Link zum Volltext

Quelle

EZB-FREE-00999 freely available EZB journals

Beschreibungen/Notizen

• Background/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/dtmax). 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/dtmax 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.