Highlights
- •Limb ischemia postconditioning (LPostC) has showed the neuroprotective effects in cerebral ischemia/reperfusion rats.
- •LPostC has decreased the neuronal apoptosis in ischemia/reperfusion.
- •LPostC or SB203580 (p38 MAPK inhibitor) has inhibited the activation of p38 and ATF-2 in cerebral ischemia/reperfusion rats.
- •The neuroprotective effects of LPostC may be related to its inhibiting p38-ATF-2 pathway.
Abstract
It has been reported that remote ischemic postconditioning was able to protect from
a harmful ischemia occurring in brain. In the present study, we investigated the role
of p38 MAPK signal pathway in the process of neuroprotection and anti-apoptosis following
remote limb ischemic postconditioning on rat focal cerebral ischemia/reperfusion (I/R)
model. Male Sprague–Dawley rats were divided randomly into four groups: the sham-operated
group, I/R group, limb ischemic postconditioning (LPostC) group, and LPostC + SB203580 (p38 MAPK inhibitor) group. Focal ischemia was induced by transient middle
cerebral artery occlusion. Limb ischemic postconditioning was implemented by brief
cycles of femoral artery occlusion. At 24 h after modeling, we analyzed the neurological deficit score, assessed the cerebral
tissue morphology by H-E staining, and evaluated neuronal apoptosis by TUNEL staining.
The protein expression levels of p-p38 or p-ATF2 (phospho-activating transcription
factor 2) in the penumbra region were detected by western blotting or immunohistochemical
staining. Our findings revealed that LPostC relieved cerebral ischemia/reperfusion
injury by decreasing neurological score, improving neuronal morphological changes
in the ischemic penumbra area, and reducing neuronal apoptosis. In addition, LPostC
or LPostC + SB203580 attenuated the increase in p-p38 and p-ATF2 levels in ischemia/reperfusion
brain tissue. These results indicate that the protective effects of LPostC against
cerebral I/R injury may be related to the attenuation of neuronal apoptosis and the
suppression of p38 MAPK-ATF2 pathway.
Keywords
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Article info
Publication history
Published online: August 05, 2015
Accepted:
August 4,
2015
Received in revised form:
July 26,
2015
Received:
June 15,
2015
Identification
Copyright
© 2015 Elsevier B.V. Published by Elsevier Inc. All rights reserved.
