The Investigation Of Effect And Injury Mechanism Of Reactive Oxygen Species After Spinal Cord Injury

Objective: To explore the effect and injury mechanism of reactive oxygen species(ROS) after spinal cord injury (SCI) through detecting the change of ROS level inspinal cord after different types and degrees of SCI and observing neurocyte apoptosisand correlation apoptosis factor expression after SCIMethod: Sprague-dawley(SD) totally 204 adult female rats were randomly divided 5groups: sham goup, hemi-section, transection injury groups, light,midrange contusiongoups. The SD rats of SCI were done by Allen' s weight dropping way impact orintersection cutting on the posteriors of spinal cord T₁₀. The contents ofmalonyldialdehyed(MDA) and superoxide dissmutas(SOD) were determined bychromatometry; Limbs functional recovery was evaluate by BBB scales; Thehistopathology changing of injured spinal cord was observed by HE staining;Apoptotic cells were detected by by using terminal deoxynucleotidyl transferase2mediated dUTP nick end labeling (TUNEL) staining.The expression of Caspase-3and Bcl-2 familis in the injured spinal cord was detected by immunohistochemicalstaining.Result: 1) The concentration of MDA significantly increased and the activity of SODsignificantly descended at the 6h after different types and degrees of SCI (p＜0.05). 2)The content of MDA and SOD in the injured spinal cord tissue is not completely consistent with degree of injury following SCI. 3) The content of MDA in theinjured cord increased significantly after SCI, reached the peak at the 6h and 3 daypostinjury, then droped down gradually, then was in the normal level after 7 day; Thenumber of TUNEL labeling positive cells of SCI group increased at the 6h postinjury,reached the peak at 3-5 day, then droped down gradually, and was higher the 21postinjury than that of sham group; Bcl-2,Bax gene began increase at the 6hpostinjury, reached the peak at 5 d after injury, then droped down gradually;Caspase-3 gene began increase at the 6h postinjury, reached the peak at 3 d afterinjury, then droped down gradually;. 4) The content of MDA, the number of TUNELlabeling positive cells, the expresiong of Caspase-3 and Bax of MPSS groupdecreased significantly than that of SCI group at the same time respectively and thatof Bcl-2 improved.Conclusion: 1) The ROS in the injured cord increased significantly after differenttypes and degrees of SCI. So the ROS play a crucial role in the secondarypathological damage of SCI. 2) The level of ROS in the injured spinal cord tissue isnot completely consistent with degree of injury. 3) The primary and secondarylesion was the likely causal event that contributes to increasing of ROS in injured cordfollowing spinal cord injury. 4) ROS could possibly induce events that neurocytesin injured cord apoptosis following spinal cord injury by effecting the expresiong ofCaspase-3 and Bcl-2 family. 5) There may be many varietas of factors inducingneurocytes apoptosis in secondary lesion following spinal cord injury.