4.6 Article

Exercise preconditioning provides early cardioprotection against exhaustive exercise in rats: potential involvement of protein kinase C delta translocation

Journal

MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 368, Issue 1-2, Pages 89-102

Publisher

SPRINGER
DOI: 10.1007/s11010-012-1346-3

Keywords

Exercise preconditioning; Exhaustive exercise; Myocardial injury; Cardioprotection; Protein kinase C delta

Categories

Funding

  1. National Natural Science Foundation of China [31071031]
  2. Science and Technology Commission of Shanghai Municipality [09490503300]
  3. Shanghai Key Lab of Human Performance [11DZ2261100]

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The objective of this study was to investigate the early cardioprotective effect of exercise preconditioning (EP) on the exhaustive exercise-induced myocardial injury in rats and the role of protein kinase C delta isoform (PKC delta) in EP. Rats were subjected to run on the treadmill for four periods of 10 min each at 30 m/min with intervening periods of rest of 10 min as an EP protocol. The exhaustive exercise was performed 0.5 h after EP. PKC inhibitor chelerythrine (CHE) was injected before EP. Our results showed that EP markedly attenuated the exhaustive exercise-induced myocardial ischemia/hypoxia, ultrastructural damage, high serum cTnI, and NT-proBNP levels. CHE injection before EP did not abolish the protection of EP. Both exhaustive exercise and EP produced a significant increase in PKC delta and p-PKC delta(Thr507) protein levels in cardiomyocytes. However, the immunostaining of p-PKC delta(Thr507) in EP cardiomyocytes was primarily localized to intercalated disks and nuclei while the exhaustive exercise-induced high level p-PKC delta(Thr507) was mainly distributed in the cytoplasm. Moreover, the high PKC delta and p-PKC delta(Thr507) levels in exhaustive exercise were significantly down-regulated by EP. CHE did not attenuate the expressions of PKC delta and p-PKC delta(Thr507). These results indicate that an appropriate activation and translocation of PKC delta may represent a mechanism whereby EP can exert an early cardioprotection against exhaustive exercise-induced myocardial injury.

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