Complement factor CD59 deficiency significantly aggravates cholestasis liver injury in mice

Objective To investigate the role of complement factor CD59 in cholestatic liver injury in mouse bile duct ligation (BDL) model. Methods The cholestasis model of mice was induced by BDL. The relevant indexes were detected 3 days after operation. Results Increased alanine aminotransferase [ALT: (730.67±104.50) U/L vs. (311.33±52.47) U/L, t=8.784, P 0.05] and C5a [(284.43±80.88) μg/L vs. (212.95±13.53) μg/L, t=1.743, P>0.05] levels between the two BDL groups, suggesting that CD59 deficiency did not impact in vivo generation of C3 and C5 activation products. An increased membrane attack complex (MAC) deposition in CD59 deficiency animals could be monitored. Conclusion The present study proves a functional role of CD59 during cholestasis. CD59 deficiency leads to aggravated cholestatic liver injury by up-regulating the expression of MAC. CD59 appears to be an attractive target for future therapeutic intervention in chronic cholestatic liver disease. Key words: Cholestatic liver injury; CD59; Complement; Bile duct ligation; Membrane attack complex