LPS preconditioning mediate Nrf2 to protect spinal cord injury
10.3969/j.issn.1000-484X.2015.02.013
- VernacularTitle:LPS预处理通过Nrf2介导对脊髓损伤的保护作用
- Author:
Qingmao ZHU
;
Dianming JIANG
;
Chunyang MENG
;
Bo QIAO
;
Weichao LI
- Publication Type:Journal Article
- Keywords:
Spinal cord injury;
Lipopolysaccharide;
Preconditioning;
Oxidative stress
- From:
Chinese Journal of Immunology
2015;(2):197-203
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the neuroprotective effect and possible mechanism on rats with low dose Lipopoly -saccharide ( LPS) preconditioning after spinal cord injury.Methods:120 female SD rats were randomly divided into the empty virus (EV) group,LPS+empty virus (LPS+EV) group,Nrf2 interference virus (NIV) group,LPS+Nrf2 interference virus (LPS+NIV) group.The model of traumatic spinal cord injury ( TSCI) was established by the modified Allen′s method,motor function of the rat hind limb was assessed by the Basso Beattie and Bresnahan (BBB) score at 1,3,7,14 and 28 d after the operation.The injured spinal cord tissue samples were harvested at each time ,and the pathological changes of rat spinal cord were observed by HE staining ,the Nissl body and neuron survival index were observed by Nissl staining ,the expressions of Nrf2 and GCLC protein level were detected by immunohis-tochemical staining and Western blot.Results:The rat BBB score of LPS+EV group increased significantly than EV group at 7,14,28 d after operation ( P<0.05 ,P<0.01 );The NIV group between LPS+NIV group have no statistical significance at each time.As compared with EV group:the Nrf2 protein of LPS+EV group was expression increased significantly and Nissl staining showed that the neurons survival index was increased at 1,3 and 7 d(P<0.05,P<0.01);The GCLC protein of LPS+EV group was expression increased significantly at 1-14 d( P<0.05 );HE staining showed that the injured spinal cord pathological changes of LPS +EV group was obviously improved.Conclusion:Low dose lipopolysaccharide preconditioning can accelerate the nerve function recovery on rats with traumatic spinal cord injury ,the mechanism may be regulated by activating the Nrf 2 antioxidant stress pathway.
