Effect of corilagin on cerebral ischaemia/reperfusion-induced cerebral injury in a rat model

Abstract

Purpose: To evaluate the neuroprotective effects of corilagin in cerebral ischaemia-induced cerebral injury in a rat model. Methods: Cerebral ischaemia was induced by middle cerebral artery occlusion (MCAO). The animals were separated into five groups, including a control group that underwent surgery without inserting a monofilament; MCAO group that received saline; corilagin-treated group (20 mg/kg corilagin, intraperitoneally for 7 days after reperfusion); Tat-Beclin-1-treated group (intraperitoneal injection of 1.5mg/kg of Tat-Beclin-1 on the 3rd and 6th days after MCAO); and corilagin + Tat-Beclin-1-treated group (corilagin for 7 days and Tat-Beclin-1 on the 3rd and 6th days after MCAO). At the end of the treatments, neurological deficit, brain oedema, and volume of infarct were determined in all the animals. Moreover, the level of autophagy in infarcted tissues was evaluated by immunofluorescence, real-time PCR, and western blotting. Results: There was a significant decrease in neurological deficit, brain oedema, and volume of infarcted tissue in corilagin-treated group when compared with MCAO- and Tat-Beclin-1-treated groups. Treatment with corilagin attenuated the autophagy of astrocytes and neurons in cerebral infarcted tissue, as demonstrated by immunofluorescence, quantitative PCR, and western blotting data. Conclusion: Corlagin has a protective effect against neuronal damage in cerebral ischaemic rats by decreasing neurological deficit score, infarct volume, and water content of cerebral tissue. Corlagin attenuates autophagy in cerebral tissue, thus protecting cerebral ischaemic rats from neuronal damage.