Inhibition of classical complement activation attenuates liver ischaemia and reperfusion injury in a rat model

52Citations
Citations of this article
29Readers
Mendeley users who have this article in their library.
Get full text

Abstract

Activation of the complement system contributes to the pathogenesis of ischaemia/reperfusion (I/R) injury. We evaluated inhibition of the classical pathway of complement using C1-inhibitor (C1-inh) in a model of 70% partial liver I/R injury in male Wistar rats (n = 35). C1-inh was administered at 100, 200 or 400 IU/kg bodyweight, 5 min before 60 min ischaemia (pre-I) or 5 min before 24 h reperfusion (end-I). One hundred IU/kg bodyweight significantly reduced the increase of plasma levels of activated C4 as compared to albumin-treated control rats and attenuated the increase of alanine aminotransferase (ALT). These effects were not better with higher doses of C1-inh. Administration of C1-inh pre-I resulted in lower ALT levels and higher bile secretion after 24 h of reperfusion than administration at end-I. Immunohistochemical assessment indicated that activated C3, the membrane attack complex C5b9 and C-reactive protein (CRP) colocalized in hepatocytes within midzonal areas, suggesting CRP is a mediator of I/R-induced, classical complement activation in rats. Pre-ischaemic administration of C1-inh is an effective pharmacological intervention to protect against liver I/R injury. © 2005 British Society for Immunology.

Cite

CITATION STYLE

APA

Heijnen, B. H. M., Straatsburg, I. H., Padilla, N. D., Van Mierlo, G. J., Hack, C. E., & Van Gulik, T. M. (2006). Inhibition of classical complement activation attenuates liver ischaemia and reperfusion injury in a rat model. Clinical and Experimental Immunology, 143(1), 15–23. https://doi.org/10.1111/j.1365-2249.2005.02958.x

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free