Role of vitacamphore in improving central pro-inflammatory cytokines following transient global ischemia.

Abstract

Pro-inflammatory cytokines (PICs) including interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) are responsive to ischemic stress. This process thereby modulates the responsiveness of many cell types under diseased conditions. The current study was to examine the role played by vitacamphore (VCP) in regulating the levels of PICs and protein expression of PIC receptors in the cerebral cortex and hippocampus of rats after cardiac arrest (CA)-induced transient global ischemia. CA was induced by asphyxia followed by cardiopulmonary resuscitation (CPR) in rats. ELISA and Western blot analyses were employed to determine PICs and their receptors in the cortex and hippocampus. Our results show that IL-1β, IL-6 and TNF-α were significantly elevated in the cortex and hippocampus after CA. This was accompanied with increasing of PIC receptors, namely IL-1R, IL-6R and TNFR1. Systemic injection of VCP attenuated amplification of PIC signal pathway in these brain regions. VCP also improved Neurological Severity Score and brain tissue edema in CA rats. Notably, VCP resulted in a significant increase in survival of CA rats as compared with controls. In conclusion, VCP is likely to play a beneficial role in modulating transient global ischemia induced by CA via PIC signal mechanisms.