Neuroprotective Effects of Taurine Via Modulation of Nitric Oxide Synthase on Hypoxic-Ischemic Brain Injury in Neonatal Rats.
- Author:
Eun Jeong SONG
1
;
Yoon Yung JANG
;
Tae Yeol KIM
;
Sun Hwa CHA
;
Hye Jin PARK
;
Kye Hyang LEE
;
Kyung Hoon LEE
;
Eun Jin CHOI
;
Jin Kyung KIM
;
Hai Lee CHUNG
;
Eok Su SEO
;
Woo Taek KIM
Author Information
1. Department of Pediatrics, School of Medicine, Catholic University of Daegu, Daegu. wootykim@cu.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Taurine;
Nitric oxide synthase;
Hypoxic-ischemic
- MeSH:
Adult;
Animals;
Anoxia;
Brain;
Brain Injuries;
Carotid Arteries;
Cell Culture Techniques;
Central Nervous System;
Heart;
Humans;
Ligation;
Muscle, Skeletal;
Neurons;
Neuroprotective Agents;
Nitric Oxide;
Nitric Oxide Synthase;
Pregnancy;
Rats;
Real-Time Polymerase Chain Reaction;
Retina;
RNA, Messenger;
Taurine
- From:Korean Journal of Perinatology
2009;20(3):213-224
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Taurine is a simple sulfur-containing amino acid and enriched in brain, retina, heart and skeletal muscles. In the central nervous system, taurine has been implicated in major phenomena. Current studies have demonstrated the neuroprotective effect of taurine in adult rat model, but limited data are available for those during the neonatal periods. The aim of this study was to determine whether taurine could reduce hypoxic-ischemic (HI) brain injury in the developing brain via modulation of nitric oxide synthase. METHODS: In in vitro model, embryonic cortical neuronal cell culture procedure was done in Sprague-Dawley (SD) rats at 18 days of gestation. The cells were divided into the hypoxia group, taurine-treated group before and after a hypoxic insult. The each groups compared with normoxia group. In in vivo model, left carotid artery ligation was done in 7-day-old SD rat pups. the pups were exposed to hypoxia, received an injection of 30 mg/kg of taurine, and sacrificed at day 1, day 3, day 7, day 14 and day 28. We assayed the expression of iNOS, eNOS and nNOS mRNA using real-time PCR and western-blotting. RESULTS: In in vitro model, brain cell damage of hypoxia group was more than in the normoxia group. Cell damage's recovery was more in the taurine-treated group before a hypoxic insult than in the taurine-treated group after a hypoxic insult. The expression of iNOS mRNA was less in the hypoxia group than in the normoxia group both in vitro and in vivo models. The expression of eNOS and nNOS was more in the hypoxia group. CONCLUSION: Taurine has neuroprotective property over perinatal HI brain injury due to modulation of NOS, as evidenced by causing a decrease in eNOS and nNOS and increase in iNOS expression. The neuroprotective effect of taurine administration was maximal at day 7 and day 14 after a hypoxic injury.
