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C1-inhibitor attenuates neurobehavioral deficits following controlled cortical impact brain injury in mice

Introduction

The goal of the study was to evaluate the neurobehavioral effects of the C1-inhibitor (C1-INH), an endogenous inhibitor of complement and contact-kinin pathways, following controlled cortical impact (CCI) brain injury in mice.

Methods

Mice were anesthetized and subjected to CCI brain injury. At 10 minutes postinjury, animals randomly received an intravenous infusion of either C1-INH (15 U) or saline (equal volume, 150 μl). A second group of mice received identical anesthesia, surgery, and saline to serve as uninjured controls. The neurobehavioral motor outcome was evaluated weekly (for 4 weeks) by performing a neuroscore, and cognitive function was evaluated at 4 weeks postinjury using the Morris water maze.

Results

Consistently, brain-injured mice receiving C1-INH showed attenuated neurological motor deficits during the 4-week period compared with injured mice receiving saline (Figure 1). At 4 weeks postinjury we observed a trend towards a better cognitive performance in mice receiving C1-INH compared with mice receiving saline (n = 8 per group, P = 0.08).

figure 1

Figure 1

Conclusion

Post-traumatic administration of the endogenous complement inhibitor C1-INH significantly attenuates neurological motor deficits associated with traumatic brain injury.

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Longhi, L., Perego, C., Zanier, E. et al. C1-inhibitor attenuates neurobehavioral deficits following controlled cortical impact brain injury in mice. Crit Care 11 (Suppl 2), P358 (2007). https://0-doi-org.brum.beds.ac.uk/10.1186/cc5518

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  • DOI: https://0-doi-org.brum.beds.ac.uk/10.1186/cc5518

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