| RESEARCH ARTICLE |
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| Year : 2014 | Volume
: 46
| Issue : 2 | Page : 207-210 |
Effect of trapidil in myocardial ischemia-reperfusion injury in rabbit
MingJie Liu1, Qi Sun2, Qiang Wang3, Xiuying Wang4, Peng Lin4, Ming Yang4, Yuanyuan Yan4
1 The First Hospital of Jilin University, Changchun, Jilin 130000; Inner Mongolia University for the Nationalities, Tongliao, Inner Mongolia 028000, China
2 The First Hospital of Jilin University, Changchun, Jilin 130000; 202 Military Hospital of China, Shenyang, Liaoning 110000, China
3 202 Military Hospital of China, Shenyang, Liaoning 110000, China
4 Liaoning Provincial Institute of Food and Drug Control, Shenyang, Liaoning 110000, China
Correspondence Address:
Qi Sun
The First Hospital of Jilin University, Changchun, Jilin 130000; 202 Military Hospital of China, Shenyang, Liaoning 110000
China
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0253-7613.129320
Objectives: To evaluate the cardioprotective effects of trapidil on myocardial ischemia-reperfusion injury (MIRI) in rabbits.
Materials and Methods: Rabbits were subjected to 40 min of myocardial ischemia followed by 120 min of reperfusion. Blood for superoxide dismutase (SOD) and malondialdehyde (MDA) were estimated. At the end of reperfusion, the rabbits were sacrificed and the hearts were isolated for histological examination. An apoptotic index (AI) was determined using the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end-labeling (TUNEL) method. The expression of apoptosis-related proteins Bax and Bcl-2 was analyzed using immunohistochemistry. Statistical analyses were performed by one-way analysis of variance (ANOVA), P < 0.05 considered statistically significant
Results: Trapidil caused a significant (P < 0.05) increase in SOD activity, as decreased MDA levels and significantly (P < 0.05) reduced the expression of Bax as compared with the ischemia-reperfusion (IR) control group.
Conclusion: Trapidil may attenuate the myocardial damage produced by IR injury and offer potential cardioprotective action.
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