Safranal, a constituent of Crocus sativus (saffron), attenuated cerebral ischemia induced oxidative damage in rat hippocampus.

Increased oxidative stress has been implicated in the mechanisms of delayed neuronal cell death following cerebral ischemic insult. In this study, we investigated whether safranal, an active constituent of Crocus sativus L. stigmas, may ameliorate ischemia-reperfusion injury (IRI)-induced oxidative damage in rat hippocampus. Male NMRI rats were divided into six groups, namely, sham, control, ischemia and ischemia treated with safranal (four groups). The transient global cerebral ischemia was induced using four-vessel-occlusion method for 20 min. Safranal was injected intraperitoneally (727.5 mg/kg, 363.75 mg/kg, 145.5 mg/kg, and 72.75 mg/kg body weight) 5 min. prior to reperfusion and the administration was continued every 24 hours for 72 hours after induction of ischemia. The markers of oxidative stress including thiobarbituric acid reactive substances (TBARS), total sulfhydryl (SH) groups and antioxidant capacity of hippocampus (using FRAP assay) were measured. The transient global cerebral ischemia induced a significant increase in TBARS levels (p<0.001), decrement in both antioxidant power (FRAP value) (p<0.05) and total sulfhydryl (SH) concentrations (p<0.001) in comparison with sham-operated animals. Following safranal administration the total SH contents (3.2 vs. 0.7micromol/g, p<0.001, safranal 727.5 mg/kg) and antioxidant capacity (4.12 vs. 1.16 micromol/g, p<0.001; 727.5 mg/kg) were elevated in hippocampus in comparison with ischemic group. The MDA level was declined significantly in hippocampus (52.31 vs. 159.70 nmol/g, p<0.001; 727.5 mg/kg). It is concluded that safranal have some protective effects on different markers of oxidative damage in hippocampal tissue from ischemic rats.