Open AccessUp‐regulation of heme oxygenase‐1 by isoflurane preconditioning during tolerance against neuronal injury induced by oxygen glucose deprivation
Author(s) -
Li Qifang,
Zhu Yesen,
Jiang Hong,
Xu Hui,
Liu Heping
Publication year - 2008
Publication title -
acta biochimica et biophysica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.771
H-Index - 57
eISSN - 1745-7270
pISSN - 1672-9145
DOI - 10.1111/j.1745-7270.2008.00461.x
Subject(s) - isoflurane , heme oxygenase , heme , oxygen , oxygenase , chemistry , anesthesia , pharmacology , medicine , biochemistry , gene , enzyme , organic chemistry
Heme oxygenase (HO) is the rate‐limiting enzyme in the degradation of heme to produce bile pigments and carbon monoxide. The HO‐1 isozyme is induced by a variety of factors such as heat, heme, ischemia, and hydrogen peroxide. In recent years, mounting findings have suggested that HO‐1 has a neuroprotective activity against ischemic injury. The neuroprotective role of isoflurane, a commonly used anesthetic, has been well documented, but little is known about the underlying mechanisms involved. Recently, isoflurane has been shown to up‐regulate HO‐1 in the liver. In this study, we show that isoflurane preconditioning promotes the survival of cultured ischemic hippocampal neurons by increasing the number of surviving neurons and their viability. Further study by reverse transcription‐polymerase chain reaction and Western blot analysis showed that isoflurane preconditioning significantly increases HO‐1 expression in oxygen glucose deprivation (OGD)‐induced neuronal injury. Furthermore, inhibition of HO activity by tin protoporphyrin partially abolishes isoflurane preconditioning's protective effect as measured by lactate dehydrogenase release in OGD neurons. These findings indicated that the neuroprotective role of isoflurane preconditioning against OGD‐induced injury might be associated with its role in up‐regulating HO‐1 in ischemic neurons.