DIDS Reduces Ischemia/Reperfusion-Induced Myocardial Injury in Rats
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 chan...
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| Format: | Article |
| Language: | English |
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Cell Physiol Biochem Press GmbH & Co KG
2015-01-01
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| Series: | Cellular Physiology and Biochemistry |
| Subjects: | |
| Online Access: | http://www.karger.com/Article/FullText/369728 |
| _version_ | 1811331092144193536 |
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| author | Xiaoming Wang Yanan Cao Mingzhi Shen Bo Wang Weiwei Zhang Yan Liu Xiaole He Lin Wang Yuesheng Xia Mingge Ding Xihui Xu Jun Ren |
| author_facet | Xiaoming Wang Yanan Cao Mingzhi Shen Bo Wang Weiwei Zhang Yan Liu Xiaole He Lin Wang Yuesheng Xia Mingge Ding Xihui Xu Jun Ren |
| author_sort | Xiaoming Wang |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-04-13T16:13:40Z |
| format | Article |
| id | doaj.art-5ed12ea9c1144fe18efbda51621c3bd0 |
| institution | Directory Open Access Journal |
| issn | 1015-8987 1421-9778 |
| language | English |
| last_indexed | 2024-04-13T16:13:40Z |
| publishDate | 2015-01-01 |
| publisher | Cell Physiol Biochem Press GmbH & Co KG |
| record_format | Article |
| series | Cellular Physiology and Biochemistry |
| spelling | doaj.art-5ed12ea9c1144fe18efbda51621c3bd02022-12-22T02:40:08ZengCell Physiol Biochem Press GmbH & Co KGCellular Physiology and Biochemistry1015-89871421-97782015-01-0135267668810.1159/000369728369728DIDS Reduces Ischemia/Reperfusion-Induced Myocardial Injury in RatsXiaoming WangYanan CaoMingzhi ShenBo WangWeiwei ZhangYan LiuXiaole HeLin WangYuesheng XiaMingge DingXihui XuJun RenBackground/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.http://www.karger.com/Article/FullText/369728ApoptosisDIDSIschemia/Reperfusion injuryCardiac function |
| spellingShingle | Xiaoming Wang Yanan Cao Mingzhi Shen Bo Wang Weiwei Zhang Yan Liu Xiaole He Lin Wang Yuesheng Xia Mingge Ding Xihui Xu Jun Ren DIDS Reduces Ischemia/Reperfusion-Induced Myocardial Injury in Rats Cellular Physiology and Biochemistry Apoptosis DIDS Ischemia/Reperfusion injury Cardiac function |
| title | DIDS Reduces Ischemia/Reperfusion-Induced Myocardial Injury in Rats |
| title_full | DIDS Reduces Ischemia/Reperfusion-Induced Myocardial Injury in Rats |
| title_fullStr | DIDS Reduces Ischemia/Reperfusion-Induced Myocardial Injury in Rats |
| title_full_unstemmed | DIDS Reduces Ischemia/Reperfusion-Induced Myocardial Injury in Rats |
| title_short | DIDS Reduces Ischemia/Reperfusion-Induced Myocardial Injury in Rats |
| title_sort | dids reduces ischemia reperfusion induced myocardial injury in rats |
| topic | Apoptosis DIDS Ischemia/Reperfusion injury Cardiac function |
| url | http://www.karger.com/Article/FullText/369728 |
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