- 作者：Luwen Zhu ; MD* ; 1 ; Tao Ye ; PhDc&dagger ; ; 1 ; Qiang Tang ; MD* ; tangqiang1963@163.com" class="auth_mail" title="E-mail the corresponding author ; Yan Wang ; MD* ; Xiaojun Wu ; PhDc&dagger ; ; Hongyu Li ; MSc&dagger ; ; Yunfei Jiang ; MS&dagger ;
- 关键词：Exercise preconditioning ; cerebral ischemia/reperfusion ; TLR4/NF-κB signaling pathway ; inflammatory response
- 刊名：Journal of Stroke and Cerebrovascular Diseases
- 出版年：2016
- 出版时间：November 2016
- 年：2016
- 卷：25
- 期：11
- 页码：2770-2779
- 全文大小：1629 K
Methods
Ischemia was induced in rats using transient middle cerebral artery occlusion (tMCAO) after 3 weeks of EP. Fifty-four rats were divided into sham, MCAO, and EP+MCAO groups. Following the induction of cerebral I/R injury, rats were scored for neurological deficits. Various techniques were used to evaluate ischemic infarct volume and explore pathological changes in tissue morphology after cerebral I/R injury, wherein the levels of TLR4 and NF-κB were analyzed. In addition, enzyme-linked immunosorbent assays were used to detect the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-1β in peripheral serum.
Results
Twenty-four hours after cerebral I/R injury, the neurological deficit scores decreased and ischemic cortical damage alleviated in EP+MCAO group; the number of TLR4- and NF-κB-positive cells, the expression of TLR4 and NF-κB in the ischemic side, and the concentrations of TNF-α and IL-1β in the peripheral serum were lower in EP+MCAO group than those in the MCAO group (P < .05).
Conclusions
The present study indicates that EP can improve cerebral I/R-induced neurological deficits in rats, reduce infarct volume, mitigate pathological damage in the ischemic cortex, and exert neuroprotective effects. The mechanism underlying these effects might involve the regulation of the TLR4/NF-κB signaling pathway and the inhibition of central and peripheral inflammatory cascades during cerebral I/R injury.