Zhao Hong-Gang, Li Wen-Bin, Sun Xiao-Cai, Li Qing-Jun, Ai Ji, Li Dong-Liang
Department of Physiology, Xinxiang Medical College, Xinxiang 453003, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2007 Feb;23(1):19-23.
To explore the role of femoral nerves section (FNS) on the protection of limb ischemic preconditioning (LIP) against cerebral ischemia/reperfusion injuries.
Model 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.
Thionin 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.
Neural 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.
探讨切断股神经（FNS）对肢体缺血预处理（LIP）保护脑缺血/再灌注损伤作用的影响。
采用四动脉闭塞法制备脑缺血模型。通过夹闭双侧股动脉10分钟，间隔10分钟，重复3次来进行LIP。将永久性闭塞椎动脉的大鼠分为假手术组、脑缺血组、FNS + 脑缺血组、LIP + 脑缺血组、FNS + LIP + 脑缺血组。在假手术或脑缺血7天后，采用硫堇染色观察海马CA1区神经密度（ND）的变化。在假手术或脑缺血6小时后，采用免疫组织化学方法检测海马CA1区c-Fos的表达。
硫堇染色显示，与假手术组相比，脑缺血组和FNS + 脑缺血组海马CA1区可见严重的神经元损伤。LIP减轻了脑缺血/再灌注正常诱导的海马CA1亚区神经元损伤，LIP + 脑缺血组的ND明显高于脑缺血组（P < 0.01）。但FNS + LIP + 脑缺血组海马CA1亚区出现明显的神经元损伤，与LIP + 脑缺血组相比，ND明显降低（P < 0.01）。这些结果表明，预先切断股神经可能会取消LIP对脑缺血/再灌注损伤的保护作用。发现假手术组海马CA1区几乎没有c-Fos表达。脑缺血组海马CA1亚区c-Fos表达变化与假手术组相似。但在LIP + 脑缺血组，海马CA1亚区c-Fos表达明显增加，阳性细胞数量和c-Fos表达光密度均明显高于假手术组和脑缺血组。FNS + LIP + 脑缺血组海马CA1亚区c-Fos表达再次降低，阳性细胞数量和c-Fos表达光密度均明显低于LIP + 脑缺血组。
神经通路参与了LIP对脑的保护作用，脑缺血/再灌注后LIP使海马CA1区c-Fos表达增加，可能是LIP诱导脑缺血耐受的神经通路的一部分。
