Caspase inhibitor affords neuroprotection with delayed administration in a rat model of neonatal hypoxic-ischemic brain injury - PubMed (original) (raw)

Caspase inhibitor affords neuroprotection with delayed administration in a rat model of neonatal hypoxic-ischemic brain injury

Y Cheng et al. J Clin Invest. 1998.

Abstract

Programmed cell death (apoptosis) is a normal process in the developing nervous system. Recent data suggest that certain features seen in the process of programmed cell death may be favored in the developing versus the adult brain in response to different brain injuries. In a well characterized model of neonatal hypoxia-ischemia, we demonstrate marked but delayed cell death in which there is prominent DNA laddering, TUNEL-labeling, and nuclei with condensed chromatin. Caspase activation, which is required in many cases of apoptotic cell death, also followed a delayed time course after hypoxia-ischemia. Administration of boc-aspartyl(OMe)-fluoromethylketone, a pan-caspase inhibitor, was significantly neuroprotective when given by intracerebroventricular injection 3 h after cerebral hypoxia-ischemia. In addition, systemic injections of boc-aspartyl(OMe)-fluoromethylketone also given in a delayed fashion, resulted in significant neuroprotection. These findings suggest that caspase inhibitors may be able to provide benefit over a prolonged therapeutic window after hypoxic-ischemic events in the developing brain, a major contributor to static encephalopathy and cerebral palsy.

PubMed Disclaimer

Comment in

Similar articles

Cited by

References

    1. EMBO J. 1992 Feb;11(2):619-27 - PubMed
    1. Ann Neurol. 1986 Feb;19(2):105-11 - PubMed
    1. Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):2007-12 - PubMed
    1. Int Rev Cytol. 1980;68:251-306 - PubMed
    1. Nat Med. 1997 Sep;3(9):954-5 - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources