2009Acta Academiae Medicinae XuzhouRequires access

Effect of isoflurane on focal cerebral ischemia/reperfusion-induced phosphorylation of c-Jun in rats

Guangyi Zhang

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Abstract

Objective To observe the focal cerebral ischemia/reperfusion-induced phosphorylation of c-Jun in rats and investigate the effect of isoflurane.Methods Animal model of global cerebral ischemia was established by ligation of bilateral common carotid and vertebral arteries(four vessels).Healthy male Sprague-Dawley rats were randomly divided into four groups: sham operation group(S),ischemia/reperfusion group(I/R),2 h 1.5 MAC isoflurane preconditioning+ischemia/reperfusion group(I/R+Iso) and 2 h pure O2 inhalation+ischemia/reperfusion group(I/R+O2).15 min after global cerebral ischemia,the rats were allowed 6 hours of reperfusion.Determination of phosphorylation of c-Jun was performed by Western blotting and immunohistochemistry.Results The phosphorylation levels of c-Jun in I/R+Iso group was markedly lower than that in I/R and I/R+O2 groups(P0.05).Conclusion Isoflurane is able to inhibit the phosphorylation of c-Jun,which might be one of its protective mechanisms in the ischemia/reperfusion-induced brain injuries in rats.

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Objective To observe the focal cerebral ischemia/reperfusion-induced phosphorylation of c-Jun in rats and investigate the effect of isoflurane.Methods Animal model of global cerebral ischemia was established by ligation of bilateral common carotid and vertebral arteries(four vessels).Healthy male Sprague-Dawley rats were randomly divided into four groups: sham operation group(S),ischemia/reperfusion group(I/R),2 h 1.5 MAC isoflurane preconditioning+ischemia/reperfusion group(I/R+Iso) and 2 h pure O2 inhalation+ischemia/reperfusion group(I/R+O2).15 min after global cerebral ischemia,the rats were allowed 6 hours of reperfusion.Determination of phosphorylation of c-Jun was performed by Western blotting and immunohistochemistry.Results The phosphorylation levels of c-Jun in I/R+Iso group was markedly lower than that in I/R and I/R+O2 groups(P0.05).Conclusion Isoflurane is able to inhibit the phosphorylation of c-Jun,which might be one of its protective mechanisms in the ischemia/reperfusion-induced brain injuries in rats.

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Available abstract

Objective To observe the focal cerebral ischemia/reperfusion-induced phosphorylation of c-Jun in rats and investigate the effect of isoflurane.Methods Animal model of global cerebral ischemia was established by ligation of bilateral common carotid and vertebral arteries(four vessels).Healthy male Sprague-Dawley rats were randomly divided into four groups: sham operation group(S),ischemia/reperfusion group(I/R),2 h 1.5 MAC isoflurane preconditioning+ischemia/reperfusion group(I/R+Iso) and 2 h pure O2 inhalation+ischemia/reperfusion group(I/R+O2).15 min after global cerebral ischemia,the rats were allowed 6 hours of reperfusion.Determination of phosphorylation of c-Jun was performed by Western blotting and immunohistochemistry.Results The phosphorylation levels of c-Jun in I/R+Iso group was markedly lower than that in I/R and I/R+O2 groups(P0.05).Conclusion Isoflurane is able to inhibit the phosphorylation of c-Jun,which might be one of its protective mechanisms in the ischemia/reperfusion-induced brain injuries in rats.

Key concepts: Isoflurane, Ischemia, Phosphorylation, Medicine, Ligation, Anesthesia, Reperfusion injury, Internal medicine

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