Protective effect of S-allyl cysteine against cerebral ischemia/reperfusion injury in experimental rats

Abstract

Purpose: To investigate the protective effect of S-allyl cysteine (SAC) against cerebral ischemia reperfusion injury (CRI) in rats. Methods: The protective effect of SAC was determined in a male Wistar rat model of middle cerebral artery occlusion (MCAO)-stimulated transient focal ischemia, followed by reperfusion. Cerebral ischemia reperfusion injury was induced via 90 min of MCAO, followed by 24-h reperfusion. The cerebral infarct size was determined by staining with 2,3,5- triphenyl tetrazolium chloride. The onset of cellular derangement, neurological deficit score and neuronal oedema were determined. In addition, the expressions of CRI markers and inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA). Results: Rats subjected to CRI showed marked increases in cellular oxidative stress, as evidenced by significant increase in the levels of inflammatory markers, including MDA (p < 0.05), MPO (p < 0.05) and nitric oxide (p < 0.01). In addition, CRI increased the mRNA expression levels of the marker genes TLR4, syndecan-1, CSF, aquaporin-1, OCT3, and RFX1. In contrast, rats pre-treated with SAC prior to CRI displayed reduced levels of inflammatory cytokines, with a near-normal cellular arrangement. SAC treatment significantly reduced the mRNA expression levels of the marker genes in CRI rats. Conclusion: These findings suggest that SAC may protect the brain of rats from cerebral ischemiareperfusion injury caused by amplification of oxidative stress and inflammatory signaling. Thus, S-allyl cysteine is a potential therapy for the management of CRI.