Citation

Wen YT, Liu TT, Lin YF, Chen CC, Kung WM, Huang CC, Lin TJ, Wang YH, Wei L. Int. J. Med. Sci. 2015; 12(9): 737-741.

Affiliation

1. Department of Neurosurgery, Taipei Medical University-Wan Fang Hospital, Taipei 11696, Taiwan ; 10. The PhD Program of Translational Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.

Copyright

(Copyright © 2015, Ivyspring International Publisher)

DOI

10.7150/ijms.12517

PMID

26392811

Abstract

Exposure to high environmental temperature leading to increased core body temperature above 40°C and central nervous system abnormalities such as convulsions, delirium, or coma is defined as heat stroke. Studies in humans and animals indicate that the heat shock responses of the host contribute to multiple organ injury and death during heat stroke. Heme oxygenase-1 (HO-1)-a stress-responsive enzyme that catabolizes heme into iron, carbon monoxide, and biliverdin-has an important role in the neuroprotective mechanism against ischemic stroke. Here, we investigated the role of endogenous HO-1 in heat-induced brain damage in rats. RT-PCR results revealed that levels of HO-1 mRNA peaked at 0 h after heat exposure and immunoblot analysis revealed that the maximal protein expression occurred at 1 h post-heat exposure. Subsequently, we detected the HO-1 expression in the cortical brain cells and revealed the neuronal cell morphology. In conclusion, HO-1 is a potent protective molecule against heat-induced brain damage. Manipulation of HO-1 may provide a potential therapeutic approach for heat-related diseases.

Language: en