Abstract: Objective To study the effect of luteolin on alleviating cerebral ischemia reperfusion injury in rats and its potential mechanism. Methods SD rats were randomly divided into the sham operation group, the middle cerebral artery occlusion (MCAO) group, the low dose luteolin group (50 mg/kg), the high dose luteolin group (100 mg/kg) and the nimodipine group (15 mg/kg). Rats were administered orally for 7 days. MCAO rat model was established by the method of wire bolt. Changes of neurological function injury score, brain tissue water content, cerebral infarct volume, tumor necrosis factor α (TNF- α), interleukin 6 (IL-6), interleukin 1β (IL-1β), B-cell lymphoma factor 2 (Bcl-2), Bcl-2 associated X protein (Bax) and Caspase-3 contents, and phosphorylated Janus protein tyrosine kinase 2 (p-JAK2) and phosphorylated signal transduction and transcriptional activation protein 3 (p-STAT3) protein expression were compared between groups. Results Neurological function injury score, brain tissue water content, cerebral infarct volume, TNF-α, IL-6, IL-1β, Bax and Caspase-3 contents, and JAK2 and STAT3 protein phosphorylation levels were significantly increased in the MCAO group compared with the sham operation group (P＜0.05), while Bcl-2 content was significantly decreased (P＜0.05). Compared with the MCAO group, neurological function injury score, brain tissue water content, cerebral infarct volume, TNF-α, IL-6, IL-1β, Bax and Caspase-3 contents, and JAK2 and STAT3 protein phosphorylation levels were significantly decreased in the low and high dose luteolin groups and the nimodipine group (P＜0.05), while Bcl-2 content was significantly increased (P＜0.05). Conclusion Luteolin can alleviate cerebral ischemia reperfusion injury in rats, which is related to the inhibition of JAK2/STAT3 signaling pathway, thereby reducing inflammatory response and apoptosis.

Key words: luteolin, reperfusion injury, brain ischemia, inflammation, apoptosis, Janus kinase 2, STAT3 transcription factor