Effect of Allopurinol on Myocardial Energy Metabolism in Chronic Heart Failure Rats After Myocardial Infarct
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- Wang Zhenzhen
- Department of Cardiology, Second Affiliated Hospital, Chongqing Medical University
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- Ding Juan
- Department of Cardiology, Second Affiliated Hospital, Chongqing Medical University
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- Luo Xiang
- Department of Cardiology, Second Affiliated Hospital, Chongqing Medical University
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- Zhang Siliang
- Department of Cardiology, Second Affiliated Hospital, Chongqing Medical University
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- Yang Gang
- Department of Cardiology, Second Affiliated Hospital, Chongqing Medical University
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- Zhu Que
- Department of Cardiology, Second Affiliated Hospital, Chongqing Medical University
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- Liu Dichuan
- Department of Cardiology, Second Affiliated Hospital, Chongqing Medical University
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抄録
<p>To determine the effect of the xanthine oxidase (XO) inhibitor allopurinol on myocardial energy metabolism in a chronic heart failure rat model after myocardial infarct.</p><p>An AMI model was established in 6-week-old rats via the ligation of the anterior descending coronary artery. Thirty-five rats were randomly divided into the following 3 groups: an ALLO group, an AMI group, and a Sham group. Heart failure was successfully diagnosed via echocardiography and blood tests. Xanthine oxidase (XO), malondialdehyde (MDA), PGC-1α, CPT-1, and GLUT4 were monitored in the myocardium.</p><p>The TEM results demonstrated that myofilament lysis and mitochondrial swelling were alleviated in the ALLO group compared with the AMI group (without ALLO). The results also demonstrated that cardiac function was significantly improved in the ALLO group compared with the AMI group. Compared with the AMI group, the ALLO group exhibited increased respiratory-chain enzyme activity, as well as increased PGC-1α and CPT-1 mRNA and protein expression, decreased MDA content, and decreased XO and GLUT4 mRNA and protein expression.</p><p>ALLO improves myocardial energy metabolism in rats with chronic heart failure, which may result from the regulation of PGC-1α in the setting of glycolipid metabolism, enhancing the production of ATP.</p>
収録刊行物
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- International Heart Journal
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International Heart Journal 57 (6), 753-759, 2016
一般社団法人 インターナショナル・ハート・ジャーナル刊行会