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Fructose-1,6-bisphosphate after hypoxic ischemic injury is protective to the neonatal rat brain
A Sola1, M Berrios, R A Sheldon
1Department of Pediatrics (Neonatology), University of California, San Francisco 94143-0734, USA. asola@peds.ucsf.edu
Insights
Fructose-1,6-bisphosphate (FBP) protects neonatal rat brains from hypoxia-ischemia injury. This treatment significantly reduced brain damage and severe injury in developing brains following ischemic-hypoxic insults.
Area of Science:
- Neuroscience
- Biochemistry
- Developmental Biology
Background:
- Fructose-1,6-bisphosphate (FBP) demonstrates neuroprotective effects in adult animal models.
- Hypoxia-ischemia (HI) is a critical condition causing central nervous system (CNS) injury in newborns.
Purpose of the Study:
- To investigate the protective efficacy of FBP against CNS injury in a neonatal rat model of HI.
- To determine if FBP administration post-insult can mitigate brain damage in developing brains.
Main Methods:
- Neonatal rats (postnatal day 7) underwent focal ischemia followed by global hypoxia.
- Animals received either FBP or saline intraperitoneally after the insult.
- Quantification of brain injury, including infarct volume and cortical damage, was performed.
Main Results:
- FBP administration (≥500 mg/kg) significantly reduced overall brain injury compared to saline.
- FBP treatment led to a substantial decrease in severe brain damage and infarct size.
- Fewer FBP-treated rats exhibited extensive ipsilateral cortical injury.
Conclusions:
- Systemic FBP treatment administered after hypoxia-ischemia effectively reduces CNS injury in neonatal rats.
- FBP shows promise as a therapeutic agent for neonatal brain protection following ischemic events.
- Further research into FBP's mechanism, including its effect on serum calcium, is warranted.
Abstract:
Fructose-1,6-bisphosphate (FBP) has been shown to attenuate central nervous system injury in adult animals. We evaluated whether FBP given after an ischemic-hypoxic insult is protective to the developing brain in a neonatal rat model of hypoxia-ischemia. Postnatal day 7 rat pups were subjected to focal ischemia followed by global hypoxia and then administered either FBP or saline intraperitoneally. A dose of 500 mg/kg or greater of FBP significantly reduced the amount of injury such that 55% of FBP- vs. 17% of saline-treated rats had no injury; 6% of FBP- and 47% of saline-treated rats had severe damage (P = 0.004). There was less infarcted brain in FBP-treated rats (12 +/- 11% vs. 37 +/- 32%; P = 0.005); and fewer FBP-treated rats had > 30% ipsilateral cortical injury (12% of FBP- vs. 50% of saline-treated rats; P = 0.002). FBP lowered serum calcium levels during the first 24 h after the insult without significant changes in ionized calcium or osmolarity. These results indicate that FBP treatment administered systemically after hypoxia-ischemia reduces CNS injury in neonatal rats.