title: The role of inducible nitric oxide synthase following spinal cord injury in rat.
abstract: Acute spinal cord injury (SCI) is two-step process that first involves the primary mechanical injury and then the secondary injury is induced by various biochemical reactions. Apoptosis is one of secondary SCI mechanisms and it is thought to play an important role for the delayed neuronal injury. The enhanced formation of nitric oxide (NO) via inducible nitric oxide synthase (iNOS) has been implicated in the pathogenesis of apoptosis in SCI. The level of .iNOS mRNA peaked at 6 hr after SCI and it declined until 72 hr after SCI in a rat model. Double-immunofluorescence staining revealed that iNOS positive cells were stained for ED-1, synaptophysin, GFAP, and oligodendrocyte marker. The terminal deoxynucleotidyl-transferase-mediated dUDP-biotin nick end-labeling (TUNEL) positive cell count was higher for the 72 hr post-SCI group than for the 24 hr post-SCI group. This cell count was also higher going in the caudal direction than in the rostral direction from the epicenter, and especially for the 72 hr group. Treatment with a selective iNOS inhibitor resulted in the reduction of TUNEL-positive cells at the lesion site. These findings suggest that nitric oxide generated by the iNOS of macrophages, neurons, oligodentrocytes, and astrocytes plays an important role for the acute secondary SCI that results from apoptotic cell death.
authors.affiliation: Department of Oral Pathology, School of Medicine, Kyungpook National University, Daegu, Korea.
authors.forename: Eun Kyoung
authors.initials: EK
authors.lastname: Kwak
authors.forename: Jung Wan
authors.initials: JW
authors.lastname: Kim
authors.forename: Ku Seong
authors.initials: KS
authors.lastname: Kang
authors.forename: Yoon Hee
authors.initials: YH
authors.lastname: Lee
authors.forename: Quan Hong
authors.initials: QH
authors.lastname: Hua
authors.forename: Tae In
authors.initials: TI
authors.lastname: Park
authors.forename: Ji Young
authors.initials: JY
authors.lastname: Park
authors.forename: Yoon Kyung
authors.initials: YK
authors.lastname: Sohn
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D017209:Apoptosis; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D020287:In Situ Nick-End Labeling; D008856:Microscopy, Fluorescence; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013116:Spinal Cord / Q000737:chemistry / Q000201:enzymology / Q000473:pathology; D013119:Spinal Cord Injuries / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D013997:Time Factors
chemical_list: D005904:Glial Fibrillary Acidic Protein; D012333:RNA, Messenger