Abstract: Objective To observe the effects of mannitou on nerve injury, inflammation, oxidative stress and neuronal apoptosis in brain tissue of rats with ischemia-reperfusion, and to explore the relationship between its potential mechanism and mitogen-activated protein kinase (MAPK) signaling pathway. 
Methods The model of cerebral ischemia-reperfusion injury in rats was established by thread occlusion method. Sixty rats were randomly divided into sham operation group, model group, mannitou group and mannitou+metformin group. The nerve defect, brain water content, cerebral stroke rate and pathological injury of hippocampus were detected. Serum tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), superoxide dismutase (SOD), and malondialdehyde (MDA) were detected by enzyme-linked immunosorbent assay (ELISA). TdT mediated dUTP nick end labeling (TUNEL) was used to detect neuronal apoptosis in brain tissue, and the phosphorylated (p)-p38 mitogen-activated protein kinase (p38), extracellular regulated protein kinase 1/2 (ERK1/2), p38 and ERK1/2 proteins were detected by Western blot (WB). 
Results Compared with the sham operation group, the model group had increased neurological deficit score, brain water content, cerebral stroke rate and neuron apoptosis rate, aggravated pathological injury of neurons, and increased serum TNF-α, IL-6 and MDA increased, decreased SOD, and increased expression of p-p38 and p-ERK1/2 protein in brain (P＜0.05). After administration of mannitou, the above indexes of rats were significantly and reversely regulated, and this effect of mannitou could be weakened by metformin. 
Conclusion Mannitou could reduce the brain nerve injury induced by ischemia-reperfusion in rats, and inhibit brain inflammation, oxidative stress and neuronal apoptosis, thus protecting the brain. The mechanism may be related to the inhibition of the activity of MAPK signaling pathway.

Key words: reperfusion injury, mannitol, oxidative stress, inflammation