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Possible protective role of growth hormone in hypoxia-ischemia in neonatal rats
K Gustafson1, H Hagberg, B A Bengtsson
1Institute of Obstetrics and Gynecology, Department of Internal Medicine, Sahlgrenska University Hospital, Göteborg, Sweden.
Insights
Perinatal asphyxia causes brain injury. Growth hormone (GH) and insulin-like growth factor-I (IGF-I) show neuroprotective effects in neonatal rats after hypoxic-ischemic brain injury, suggesting their role in recovery.
Area of Science:
- Neuroscience
- Developmental Biology
- Endocrinology
Background:
- Perinatal asphyxia is a significant cause of neonatal neurologic morbidity.
- Hypoxic-ischemia (HI) models are crucial for studying brain injury mechanisms.
- Growth factors, like IGF-I, have demonstrated neuroprotective potential in HI models.
Purpose of the Study:
- To investigate the time course of mRNA expression for IGF-I, IGF-I receptor, and GH receptor following HI in neonatal rats.
- To evaluate the neuroprotective efficacy of GH administration in a neonatal rat model of HI brain injury.
Main Methods:
- Solution hybridization was used to quantify mRNA levels of IGF-I, IGF-I receptor, and GH receptor.
- Neonatal rats (7-day-old) were subjected to HI.
- GH was administered subcutaneously at doses of 50 and 100 mg/kg post-HI.
Main Results:
- IGF-I mRNA levels significantly increased in the damaged hemisphere at 72 hours and 14 days post-HI.
- In the contralateral hemisphere, both IGF-I and GH receptor mRNA levels increased by 14 days post-HI.
- GH administration provided moderate neuroprotection (20%) against HI brain injury.
Conclusions:
- The GH/IGF-I axis plays a role in the neurochemical processes underlying HI brain injury.
- These findings suggest potential therapeutic targets for mitigating perinatal asphyxia-related brain damage.
- Further research into GH/IGF-I signaling could lead to novel interventions for neonatal brain injury.
Abstract:
Perinatal asphyxia still constitutes a clinical hazard associated with considerable neurologic morbidity. Several growth factors, including insulin-like growth factor-I (IGF-I), have been reported to have a neuroprotective effect in experimental models of hypoxic ischemia (HI). In the present study, we have applied solution hybridization for quantification of the time course for mRNA expression of IGF-I, IGF-I receptor, and growth hormone (GH) receptor after HI in 7-d-old rats. There was a significant increase in IGF-I mRNA in the damaged hemisphere 72 h (1.19 +/- 0.28 vs 0.48 +/- 0.02 amol/microg DNA, p < 0.05) and 14 d (0.61 +/- 0.18 vs 0.19 +/- 0.05 amol/microg DNA, p < 0.05) after HI. In the contralateral hemisphere, both IGF-I and GH receptor mRNA had increased by 14 d after the insult (0.36 +/- 0.042 vs 0.13 +/- 0.011, p < 0.05, and 0.31 +/- 0.013 vs 0.11 +/- 0.004 amol/microg DNA, p < 0.001, respectively). There were no changes in IGF-I receptor mRNA throughout the study period. We have also evaluated the neuroprotective effect of GH after HI in neonatal rats. GH administered s.c. after HI in daily doses of 50 and 100 mg/kg provided a moderate neuroprotection of 20%. These results suggest a role for the GH/IGF-I axis in the neurochemical process leading to HI brain injury.