Produced By Ischemia Reperfusion By

When the SMS was administered to rats either before or after cerebral ischemia reperfusion, oxidative damage in the brain was markedly prevented as evaluated by two biochemical indications, thiobarbiturate reactive substance (TBARS) formation and glutathione peroxidase (GPX) activity (10,11).

The same protective effect of SMS was shown against brain oxidative damage in mice as well as in rats. Figure 2 shows the preventive effect of SMS on brain oxidative injury induced by ischemia reperfusion in C57BL/6 mice. The mice were administered SMS directly into the duodenum 2 hr before ischemia produced by the occlusion of both right and left common carotid arteries exposed through a middle skin incision for 85 min. At the end of the ischemic period, carotid arteries were declamped to allow blood reperfusion for 45 min. The both TBARS formation and GPX activity were measured in isolated brain homogenate. After the ischemia reperfusion, TBARS formation was increased to approximately 260% of untreated control but the formation was almost completely inhibited by the administration of SMS

Figure 2 Inhibitory effects of SMS on TBARS formation and GPX activity loss in mouse brain after ischemia-reperfusion.

prior to ischemia treatment. GPX activity, on the other hand, decreased to approximately 46% of vehicle control after ischemia reperfusion but this decline was also effectively prevented by SMS preadministration (recovered to 84% of control). This SMS effect was completely dose-dependent for both the inhibition of TBARS formation and GPX activity loss; furthermore, TTC (2,3,5-trimethyl tetrazolium chloride) staining of the brain slices confirmed the preventive effect of SMS on cerebral oxidative injury caused by ischemia reperfusion (11) (Fig. 3). Recently, we also studied the effect of SMS on

Anterior

SMS-treated

Figure 3 Protective effect of SMS against cerebral ischemia-reperfusion injury in rats evaluated by TTC staining.

Anterior

SMS-treated

Figure 3 Protective effect of SMS against cerebral ischemia-reperfusion injury in rats evaluated by TTC staining.

cerebral oxidative damage caused by MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) administration in a Parkinson's disease model in mice and found that the oxidative injury in the substantia nigra was sufficiently inhibited by orally administered SMS (12).

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