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Journal of the Korean Pediatric Society 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 Lee1, Sang-Hyun Byun2, Ren Zhe Ann3, Kyu-Sang Song4, Young-Ik Lee5, Yoo-Jung Hahn5, Yong-Hun Chung2
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
신생 백서에서 IGF-I 투여가 저산소성 허혈성 뇌병증에 관련된 유전자 발현에 미치는 효과
이형신1, 변상현2, 안인철3, 송규상4, 이영익5, 한유정5, 정용헌2
1가톨릭대학교 의과대학 소아과학교실
2충남대학교 의과대학 소아과학교실
3중국연변대학 의학원 소아과학교실
4충남대학교 의과대학 조직병리학교실
5생명과학연구부
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.
Key Words: IGF-I, Apoptosis, Hypoxic ischemic brain injury, Bax, Bcl-2


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