Study Design. Experimental animal study.
Objective. This study investigated whether nitric oxide (NO) mediated protein nitration is involved in the pathogenesis of radiculopathy and whether the symptoms can be relieved by its suppression.
Summary of Background Data. It has been reported that nitration of protein mediated by NO is involved in the degenerative neurological disorders, but its involvement is not clear in the radiculopathy.
Methods. Two kinds of rat models of radiculopathy were used. Radiculopathy was induced either by ligation of spinal nerve roots or transplantation of autologous nucleus pulposus. In separate groups of rats, aminoguanidine, a potent nitric oxide synthetase inhibitor, was administered just before induction of radiculopathy, to suppress NO production and resultant nitration of protein. Sensation of the hind limb was evaluated by plantar stimulation test, and motor weakness was assessed by observation of gait pattern. Nitrotyrosine, product of protein nitration, was assayed quantitatively by Western immunoblotting.
Results. Mechanical allodynia was observed in both compression and nucleus pulposus groups, but motor weakness was observed only in the compression group. Preoperative administration of aminoguanidine attenuated mechanical allodynia and motor weakness. Optical densities of nitrotyrosine bands increased significantly in radiculopathy groups, but they were lowered by administration of aminoguanidine.
Conclusion. NO mediated protein nitration contributes to the development of both types of radiculopathies. Suppression of NO production can decrease protein nitration and relieve neural dysfunctions of radiculopathy.
Level of Evidence: N/A
Radiculopathy was induced in rats either by ligation of spinal nerve roots or nucleus pulposus autograft. Mechanical allodynia was significantly decreased by aminoguanidine (P < 0.05). Optical densities of nitrotyrosine bands were also lowered significantly (P < 0.05). Inhibition of nitric oxide production results in decreased protein nitration and neural dysfunctions.
From the Departments of *Rehabilitation Medicine and
†Biochemistry, Dankook University College of Medicine, Cheonan, Choongnam, Republic of Korea; and
‡Institute of Tissue Regeneration Engineering (ITREN), Dankook University, Cheonan, Choongnam, Republic of Korea.
Address correspondence and reprint requests to Seong Jae Lee, MD, PhD, Department of Rehabilitation Medicine, Dankook University Hospital, San 16-5, Anseo-dong, Cheonan, Choongnam 330-715, Republic of Korea; E-mail: firstname.lastname@example.org
Acknowledgment date: April 8, 2013. Revision date: May 30, 2013. Acceptance date: June 7, 2013.
The device(s)/drug(s) that is/are the subject of the manuscript do not apply to human subjects.
Dankook University research funds were received to support this work.
No relevant financial activities outside the submitted work.