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Year : 2016  |  Volume : 2  |  Issue : 3  |  Page : 123-130

Primary Screening for Proteins Differentially Expressed in the Myocardium of a Rat Model of Acute Methamphetamine Intoxication

1 Hubei Chongxin Forensic Identification Centre, Wuhan, Hubei 430000, China
2 Department of Forensic Medicine, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, China
3 Key Laboratory of Evidence Science, China University of Political Science and Law, Ministry of Education; Collaborative Innovation Center of Judicial Civilization, Beijing, Haidian 100192, China

Correspondence Address:
Haidong Zhang
Key Laboratory of Evidence Science (China University of Political Science and Law), Ministry of Education, Beijing, Haidian 100192, China; Collaborative Innovation Center of Judicial Civilization, Beijing, Haidian 100192
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2349-5014.191460

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The mechanism of myocardial injury induced by the cardiovascular toxicity of methamphetamine (MA) has been shown to depend on alterations in myocardial proteins caused by MA. Primary screening of the expression of myocardial proteins in a rat model of MA intoxication was achieved by combining two-dimensional electrophoresis and mass spectrometry analyses, which revealed a total of 100 differentially expressed proteins. Of these, 13 displayed significantly altered expression. Moreover, Western blotting and real-time reverse transcription quantitative polymerase chain reaction analyses of several relative proteins demonstrated that acute MA intoxication lowers protein expression and mRNA transcription of aldehyde dehydrogenase-2 and NADH dehydrogenase (ubiquinone) 1 alpha subcomplex subunit 10. In contrast, MA intoxication elevated the protein expression and mRNA transcription of heat shock protein family B (small) member 1. By combining behavioral assessments of experimental rat models with the histological and pathological changes evident in cardiomyocytes, a mechanism accounting for MA myocardial toxicity was suggested. MA alters the regulation of gene transcription and the subsequent expression of certain proteins that participate in myocardial respiration and in responding to oxidative stress, resulting in myocardial dysfunction and structural changes that affect the functioning of the cardiovascular system.

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