CVF
CVF improved blood flow and clinical outcome following cerebral ischemia with reperfusion (Vasthare et al., 1998) CVF improved cerebral blood flow and significant return of somatosensory evoked potentials (D'Ambrosio et al., 2001). CVF administration significantly reduced post-ischemic cerebral infarct and atrophy in adult and neonatal rats (Figueroa et al., 2005). CVF- complement-depleted rabbits were no different from the control group receiving no therapy (Lew et al., 1999). CVF did not reduce the neuronal loss, edema, or atrophy in 21 days old rats (Lassiter et al., 2001). CVF did not eliminate complement deposition within the injured neonatal rat brain (Cowell et al., 2003).
|
C1 Inhibition
Administration of C1-INH had a significant protective effect against infarct development (Heimann et al., 1999). C1-INH-treated mice had reduced leukocyte infiltration (De Simoni et al., 2003). No decrease in infarct volume in C1q−/− mice compared to wild types (De Simoni et al., 2003). C1-INH reduced expression of the adhesion molecules and pro-inflammatory cytokines induced by the ischemia (De Simoni et al., 2003). BSF468248, a novel potent C1-INH, was not effective against cerebral ischemia (Kaido et al., 2003). C1-INH markedly inhibited the activation and/or recruitment of microglia/macrophages (Storini et al., 2005). C1-INH has a strong neuroprotective effect independent from C1q-mediated activation of classical pathway (Storini et al., 2005). C1q deletion had no effect against cerebral infarct development (Mocco et al., 2006a).
|
C3 Inhibition
sCR1-treated animals showed smaller infarct volumes and improved CBF (Huang et al., 1999). sCR1sLex which was also able to inhibit selectin-mediated adhesion (Huang et al., 1999). Molecular hybrid of sCR1 did not affect the cerebral infarct volume compared to controls in 7 days old neonatal rats (Imm et al., 2002). Modest cerebral protection by sCR1 in adult mice (Mocco et al., 2006a; Mocco et al., 2006b). C3−/− mice demonstrated significant reductions in both infarct volume and neurological deficit score (Mocco et al., 2006a). C3−/− mice also manifested decreased granulocyte infiltration and reduced oxidative stress (Mocco et al., 2006a). C3a-receptor antagonist SB290157 resulted in neurological improvement and stroke volume reduction (Mocco et al., 2006a). sCR1 and sCR1sLex had no effect in a primate stroke model (Ducruet et al., 2007).
|
C5 Inhibition
C5 deficient mice (C5−/−) exhibited improved functional outcome and less brain damage (Arumugam et al., 2007). C5aR antagonist did not significantly improve the stroke outcome. (Arumugam et al., 2007). C5−/− mice were not protected against I/R injury(Mocco et al., 2006a).
|
MAC Inhibition
C9 was neurotoxic and augmented the focal cerebral infarct volume (Imm et al., 2002). CD59 efficiently protects human NT2-N neurons against complement-mediated damage (Pedersen et al., 2007).
|
