Abstract
Purpose: To investigate the protective effect of S-allyl cysteine (SAC) against cerebral ischemiareperfusion 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.
Highlights
Insufficient blood flow to the brain due to certain conditions is known as cerebral ischemia
Rats pre-treated with S-allyl cysteine (SAC) before cerebral ischemia reperfusion injury (CRI) had significantly reduced infarct area and markedly low oedema, when compared with CRI rats (p < 0.001)
These findings indicate that SAC may improve neurological function following brain ischemia-reperfusion injury in rats
Summary
Insufficient blood flow to the brain due to certain conditions is known as cerebral ischemia. The lack of blood supply causes a lack of oxygen in the brain cells, leading to brain tissue death or ischemic stroke [1]. The restoration of brain blood supply as part of the treatment process induces more damage to the brain tissues after a long ischemic period This injury is known as cerebral reperfusion injury or cerebral ischemiareperfusion injury [2]. S-allyl cysteine (SAC) known for its antioxidant effects, was used in CRI rat model to protect brain tissues from reperfusion injuries. The blood marker enzymes of CRI, i.e, clusterin, neuron-specific enolase, and occludin were assayed using commercial assays kits from Abcam (USA), while KCC-positive cells were elucidated as described earlier [8]. The mRNA expression levels of the genes were calculated from the CT values, and the fold-increases were determined using the 2ΔΔCT method, with the mRNA expression value of GAPDH as the endogenous control
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