Abstract: Objective To investigate the protective effect of orexin-A (OA) on cerebral ischemia-reperfusion (I/R) injury in rats and its possible mechanism. Methods Rats were randomly divided into sham operation group (sham), ischemia-reperfusion group (I/R), 10, 30 and 50 μg/kg OA intervention group. 2,3,5-triphenylte-trazolium chloride (TTC) staining method was used to detect the cerebral infarction volume. ELISA method was used to detect the level of IL-6, TNF-α and SOD in cerebral cortex of rats, and Western blot was used to detect the expression of p-JNK. Results The I/R group had obvious infarct foci compared with the sham group, but the cerebral infarct volume significantly decreased after 30 and 50 μg/kg OA intervention (p<0.001), respectively. Compared with sham group, the levels of IL-6 and TNF-α in I / R group were significantly higher than those in sham group (p<0.05). After 30 and 50 μg/kg OA intervention, IL-6 and TNF-α levels were significantly decreased (p<0.05). The activity of SOD in I/R group was also significantly decreased (p<0.05). After 30 and 50 μg/kg OA intervention, the activity of SOD was significantly increased (p<0.05). Compared with sham group, the expression of p-JNK in I/R group was higher than that in sham group (p<0.05), yet the expression of p-JNK was decreased after 30 and 50 μg/kg OA intervention (p<0.05). Conclusion OA may play a neuroprotective role in cerebral I/R injury by inhibiting inflammatory factors and enhancing antioxidant activity.

Key words: Key words: Cerebral ischemia-reperfusion injury, Orexin-A, Inflammatory reactions, Oxidative stress