| Expression of nitric oxide synthase isoforms and N-methyl-D-aspartate receptor
subunits according to transforming growth factor-β1 administration after
hypoxic-ischemic brain injury in neonatal rats |
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Hae Young Go2, Eok Su Seo3, Woo Taek Kim1 |
2Department of Pediatrics, Gumi-Gangdong Hospital, Gumi, Gyungsangbookdo
3Department of Pediatrics, Dongguk University College of Medicine, Gyeongju, Gyungsangbookdo |
| 신생 백서의 저산소 허혈 뇌손상에서 Transforming Growth Factor-β1 투여에 따른 Nitric Oxide Synthase 이성체와 N-methyl-D-aspartate 수용체 아단위의 발현 |
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고혜영2, 서억수3, 김우택1 |
2구미강동병원 소아청소년과
3동국대학교 의과대학 안과학교실 |
Correspondence:
Woo Taek Kim, Email: wootykim@cu.ac.kr
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| Abstract |
Purpose
: Transforming growth factor (TGF)-β1 reportedly increases neuronal survival by inhibiting the induction of inducible nitric oxide synthase (NOS) in astrocytes and protecting neurons after excitotoxic injury. However, the neuroprotective mechanism of TGF-β1 on hypoxic-ischemic (HI) brain injury in neonatal rats is not clear. The aim of this study was to determine whether TGF-β1 has neuroprotective effects via a NO-mediated mechanism and N-methyl-D-aspartate (NMDA) receptor modulation on perinatal HI brain injury.
Methods
: Cortical cells were cultured using 19-day-pregnant Sprague-Dawley (SD) rats treated with TGF-β1 (1, 5, or 10 ng/mL) and incubated in a 1% O2 incubator for hypoxia. Seven-day-old SD rat pups were subjected to left carotid occlusion followed by 2 h of hypoxic exposure (7.5% O2). TGF-β1 (0.5 ng/kg) was administered intracerebrally to the rats 30 min before HI brain injury. The expressions of NOS and NMDA receptors were measured.
Results
: In the in vitro model, the expressions of endothelial NOS (eNOS) and neuronal NOS (nNOS) increased in the hypoxic group and decreased in the 1 ng/mL TGF-β1-treated group. In the in vivo model, the expression of inducible NOS (iNOS) decreased in the hypoxia group and increased in the TGF-β1-treated group. The expressions of eNOS and nNOS were reversed compared with the expression of iNOS. The expressions of all NMDA receptor subunits decreased in hypoxia group and increased in the TGF-β1-treated group except NR2C.
Conclusion
: The administration of TGF-β1 could significantly protect against perinatal HI brain injury via some parts of the NO-mediated or excitotoxic mechanism. |
| Key Words:
Transforming growth factor-β1, Hypoxia, Ischemia, Excitotoxicity, Nitric oxide synthase, N-methy1-D-aspartate receptors |
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