All issues > Volume 44(7); 2001
- Original Article
- J Korean Pediatr Soc. 2001;44(7):796-807. Published online July 15, 2001.
- IGF-I on the Expression of Gene Associated with Hypoxic Ischemic Brain Injury in the Neonatal Rats
- Hyung-Shin HS Lee1, Sang-Hyun SH Byun2, Ren Zhe RZ Ann3, Kyu-Sang KS Song4, Young-Ik YI Lee5, Yoo-Jung YJ Hahn5, Yong-Hun YH Chung2
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1Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Korea
2Department of Pediatrics, College of Medicine, Chungnam National University, Taejon, Korea
3Department of Pediatrics, College of Medicine, Yan Bian University, China
4Department of Pathology, College of Medicine, Chungnam National University, Taejon, Korea
5Life Science Research Division, Korea Research Institute of Bioscience & Biotechnology, Taejon, Korea
- Abstract
- Purpose
: To investigate the effect of intraperitoneal injection of IGF-I after hypoxic ischemic brain injury on neuronal cell necrosis, apoptosis and expression of proapoptotic and antiapoptotic proteins bax and bcl-2, respectively.
Methods
: The right carotid artery was cut between the double ligation. Then allowed to recover for 30 minutes followed by exposure to 8% oxygen at 37℃ for 2 hours. Devided 2 groups, control group(N=30) and IGF-I treated group(N=30). IGF-I treated group received IGF-I 20 μg 2 hours after hypoxic ischemic injury intraperitoneally. Rates were decapitated at 24 hours and 72 hours following hypoxic ischemic brain injury. After then, right hippocampal CA1 and CA3 neuronsof rat brains were examined.
Results
: The apoptosis and necrosis was significantly less in IGF-I treated group than control group and necrosis was more prominent in CA1 neurons than CA3 neurons. Necrosis was slightly decreased at 72 hours in both groups(P<0.05). The apoptosis was more prominent at 24 hours than 72 hours after hypoxic ischemic injury(P<0.05). Bax protein expression was prominent in control group, especially at 72 hours(P<0.05) and less in the IGF-I treated group than control group. Bcl-2 protein expression was not detected in both group.
Conclusion
: The results from this study suggest that exogenous systemic IGF-I had a neuroprotective effect by inhibition of up-regulation of bax protein expression after hypoxic ischemic brain injury.
Keywords :IGF-I, Apoptosis, Hypoxic ischemic brain injury, Bax, Bcl-2