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Treatment with IAIPs after exposure to hypoxic-ischemic brain injury decreases apoptosis


Hypoxia-Ischemia (HI) is caused by a lack of adequate blood supply to the brain, which in turn means that the brain is deprived of an adequate oxygen supply, causing an inflammatory response. Hypoxic-Ischemic Encephalopathy (HIE) is a leading cause of neurodevelopmental morbidities in new-borns, yet the only currently accepted therapeutic strategy to treat HIE is hypothermia, and even so, hypothermia is only partially protective. Thus, alternative strategies must be urgently explored. Apoptosis is defined as regulated cell death, and can be used as a hallmark of HI injury. Inter-Alpha Inhibitor Proteins (IAIPs) are novel immunomodulatory proteins that have shown some anti-inflammatory properties by decreasing neuronal degeneration in neonatal male rats that were exposed to HI injury (Threlkeld et al., Experimental Neurology, 2014). The neuroprotective effects of IAIPs on apoptosis following HI insult have not yet been studied, however, and are the focus of this study. While findings so far are only preliminary, there appears to be a protective trend for male rats. Apoptosis is shown to have increased significantly in the hippocampus, cortex and hemisphere of neonatal male rats (P<0.05).


Nakada, Sakura, "Treatment with IAIPs after exposure to hypoxic-ischemic brain injury decreases apoptosis" (2016). Summer Research Symposium. Brown Digital Repository. Brown University Library.



  • Summer Research Symposium

    Each year, Brown University showcases the research of its undergraduates at the Summer Research Symposium. More than half of the student-researchers are UTRA recipients, while others receive funding from a variety of Brown-administered and national programs and fellowships and go …