Effect of hypoxic preconditioning on neural cell apoptosis and expression of Bcl-2 and Bax in cerebral ischemia-reperfusion in rats.
In order to investigate the protective effect of hypoxic preconditioning on the cerebral ischemia-reperfusion injury, the expression of Bcl-2 and Bax was detected by using immunohistochemical staining after 3 h cerebral ischemia followed by 1, 6, 12, 24 and 48 h reperfusion respectively in rats treated with or without hypoxic preconditioning before cerebral ischemia. In addition, the apoptosis of neural cells and the behavioral scores for neurological functions recovery were evaluated by TUNEL staining and "crawling method", respectively. Compared with control group (cerebral ischemia-reperfusion without hypoxic preconditioning), the expression of Bcl-2 was significantly increased, but that of Bax decreased in the hypoxic preconditioning group (cerebral ischemia-reperfusion with hypoxic preconditioning), both P < 0.05. The pre-treatment with hypoxic preconditioning could reduce the apoptosis of neural cells and promote the neurological function recovery as compared to control group. It was suggested that hypoxic preconditioning may have protective effects on the cerebral ischemia-reperfusion injury by inhibiting the apoptosis of neural cells, increase the expression of Bcl-2 and decrease the expression of Bax.
Gao
Xiaoqun
X
Department of Anatomy, Medical College of Zhengzhou University, Zhengzhou 450052, China.
Chang
Cheng
C
Duan
Dongxiao
D
Ru
Liqiang
L
Yin
Guangfu
G
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002545:Brain Ischemia / Q000378:metabolism / Q000473:pathology*; D019194:Ischemic Preconditioning; D008297:Male; D009474:Neurons / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis* / Q000235:genetics; D051381:Rats; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology*; D051028:bcl-2-Associated X Protein / Q000096:biosynthesis* / Q000235:genetics
D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein