Nitric oxide induces macrophage apoptosis following traumatic brain injury in rats

• Published in: Neuroscience letters Vol. 339; no. 2; pp. 147 - 150
• Main Authors: Lu, Jia, Moochhala, Shabbir, Shirhan, Md, Ng, Kian Chye, Tan, Mui Hong, Teo, Ai Ling, Ling, Eng Ang
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier Ireland Ltd 20.03.2003
• Subjects: Aminoguanidine; Animals; Apoptosis; Brain Injuries - metabolism; Brain Injuries - pathology; Caspase-3; Fluorescent Antibody Technique; Guanidines - pharmacology; Inducible NO synthase; lateral fluid percussive brain injury; Macrophages - metabolism; Macrophages - pathology; Male; Nitric Oxide - metabolism; Nitric Oxide Synthase - antagonists & inhibitors; Nitric Oxide Synthase - metabolism; Nitric Oxide Synthase Type II; Percussion; Rat; Rats; Rats, Sprague-Dawley; Transferase d-UTP nick-end labeling; Inducible NO synthase; Aminoguanidine; lateral fluid percussive brain injury; Transferase d-UTP nick-end labeling; Rat; Caspase-3
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(03)00003-X

This study examined the apoptotic mechanisms of macrophages following a lateral fluid percussive brain injury. A marked induction of inducible NO synthase (iNOS) immunoexpression was observed in brain macrophages in the subarachnoid space and lateral ventricles ipsilateral to the injury. Numerous apoptotic macrophages occurred in the same region 7 days after the injury as shown by in situ terminal transferase d-UTP nick-end labeling (TUNEL) and caspase-3 immunohistochemistry. Double immunofluorescence staining showed that only a small number of TUNEL positive cells were iNOS positive; many TUNEL positive cells, however, were observed in the vicinity of iNOS positive cells. Administration of aminoguanidine resulted in a marked reduction of apoptotic cells in the lesioned area suggesting that overproduction of NO is linked to diminution of brain macrophages by apoptosis.