Email updates

Keep up to date with the latest news and content from BMC Biology and BioMed Central.

Journal App

google play app store
Open Access Research article

δ-Opioid receptor activation attenuates oxidative injury in the ischemic rat brain

Yilin Yang1*, Xiwei Xia1, Yi Zhang1, Qiang Wang1, Lu Li1, Guanghua Luo1 and Ying Xia2*

Author Affiliations

1 Third Clinical College of Schoow University, Changzhou, Jiangsu, PR China

2 Yale University School of Medicine, New Haven, Connecticut, USA

For all author emails, please log on.

BMC Biology 2009, 7:55  doi:10.1186/1741-7007-7-55

Published: 26 August 2009

Abstract

Background

We have recently shown that δ-opioid receptors (DORs) play an important role in neuroprotection from hypoxic injury via the regulation of extracellular signaling-regulated kinase (ERK) and cytochrome c release. Since ERK and cytochrome c are differentially involved in caspase signaling of oxidative injury that significantly contributes to neuronal damage in ischemia/reperfusion, we considered if DOR activation protects the ischemic brain by attenuating oxidative injury.

Results

We observed that, in a model of cerebral ischemia with middle cerebral artery occlusion, DOR activation increased the activity of major antioxidant enzymes, glutathione peroxidase and superoxide dismutase, and decreased malondialdehyde and nitric oxide levels in the cortex exposed to cerebral ischemia/reperfusion. In addition, DOR activation reduced caspase 3 expression, though it did not significantly affect the increase in interleukin (IL)1β and tumor necrosis factor (TNF)α expression at the same timepoint. PD98059, an inhibitor of mitogen-activated protein kinase (MAPK) extracellular signaling-regulated kinase kinase, accelerated animal death during ischemia/reperfusion.

Conclusion

DOR activation attenuates oxidative injury in the brain exposed to ischemia/reperfusion by enhancing antioxidant ability and inhibiting caspase activity, which provides novel insights into the mechanism of DOR neuroprotection.