Neural pathway participates in protection of limb ischemic preconditioning against brain injuries induced by ischemia/reperfusion in rats.
- Author:
Hong-Gang ZHAO
1
;
Wen-Bin LI
;
Xiao-Cai SUN
;
Qing-Jun LI
;
Ji AI
;
Dong-Liang LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Brain Ischemia; physiopathology; Extremities; blood supply; Ischemic Preconditioning; methods; Male; Neural Pathways; physiopathology; Rats; Rats, Wistar; Reperfusion Injury; physiopathology
- From: Chinese Journal of Applied Physiology 2007;23(1):19-23
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo explore the role of femoral nerves section (FNS) on the protection of limb ischemic preconditioning (LIP) against cerebral ischemia/reperfusion injuries.
METHODSModel of brain ischemia induced by Four-vessel occlusion was used. LIP was performed by clamping the bilateral femoral arteries for 10 min 3 times in a interval of 10 min. Rats with vertebral arteries permanently occluded were divided into sham group, cerebral ischemic group, FNS + cerebral ischemic group, LIP + cerebral ischemic group, FNS + LIP + cerebral ischemic group. The changes of neural density (ND) in the CA1 hippocampus were observed 7d after the sham operation or brain ischemia under thionin staining. The expression of c-Fos in the CA1 hippocampus was measured 6 h after the sham operation or brain ischemia under immunohistochemistry method.
RESULTSThionin staining revealed that serious neuronal damage was visualized in the CA1 hippocampus in both cerebral ischemic group and FNS + cerebral ischemic group as compared with sham group. LIP attenuated the neuronal damage of the CA1 subfield induced normally by cerebral ischemia/reperfusion, and ND in LIP + cerebral ischemic group was significantly higher than that in cerebral ischemic group (P < 0.01). But obvious neuronal damage of the CA1 subfield was found in FNS+ LIP + cerebral ischemic group, and ND was significantly decreased as compared with LIP + cerebral ischemic group (P < 0.01). These results suggested that the protection of LIP against cerebral ischemia/reperfusion injuries might be cancelled by preceding section of femoral nerve. It was found that there was almost no c-Fos expression in the CA1 hippocampus in sham group. Changes of c-Fos expression in the CA1 subfield in cerebral ischemic group were similar to that in sham group. But in LIP + cerebral ischemic group, c-Fos expression in the CA1 subfield was markedly increased and the number of positive cells and optical density of c-Fos expression were significantly higher than those in sham and cerebral ischemic group. c-Fos expression in the CA1 subfield was again decreased in FNS + LIP + cerebral ischemic group, and the number of positive cells and optical density of c-Fos expression were significantly lower than those in LIP + cerebral ischemic group.
CONCLUSIONNeural pathway participated in the protective effect of LIP on brain, and increased c-Fos expression in the CA1 hippocampus by LIP after cerebral ischemia/reperfusion, might be a part of neural pathway by which LIP induced brain ischemic tolerance.