Protective effect of icaritin on focal cerebral ischemic–reperfusion mice

Objective: To investigate the protective effects of icaritin(ICT),one of the active ingredients in Epimedii Folium,on mouse model of cerebral ischemia-reperfusion(I/R)in vivo.Methods: ICR mice were subjected to an 1 h transient middle cerebral artery occlusion(MCAO)and followed by 24 h of reperfusion.Neurological deficits,infarct volume,brain edema and survive rate were measured,respectively.The levels of brain IL-1β,TNF-α,ROS and DNA-binding activity of NF-κB p65 were measured by ELISA kits.The levels of malondialdehyde(MDA)and activities of superoxide dismutase(SOD)were detected by spectrophotometry,and the release of nitric oxide(NO)were detected by Griess kit.Results: ICT markedly reduced the neurological deficit scores,brain edema,infarct volume and increased the survival rate of the cerebral I/R mice.The expression of IL-1 β,TNF-α,NO,MDA and DNA-binding activity of NF-κB p65 were significantly inhibited by ICT,while the activity of SOD were up-regulated at the same time.Conclusion: ICT possessed significant neuroprotective effects in cerebral I/R mice,which might be related to prevent neuroinflammatory and oxidative damage.

Protective effect of icaritin on focal cerebral ischemic-reperfusion mice

Objective

To investigate the protective effects of icaritin (ICT), one of the active ingredients in Epimedii Folium, on mouse model of cerebral ischemia-reperfusion (I/R) in vivo.

Methods

ICR mice were subjected to an 1?h transient middle cerebral artery occlusion (MCAO) and followed by 24?h of reperfusion. Neurological deficits, infarct volume, brain edema and survive rate were measured, respectively. The levels of brain IL-1β, TNF-α, ROS and DNA-binding activity of NF-κB p65 were measured by ELISA kits. The levels of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) were detected by spectrophotometry, and the release of nitric oxide (NO) were detected by Griess kit.

Results

ICT markedly reduced the neurological deficit scores, brain edema, infarct volume and increased the survival rate of the cerebral I/R mice. The expression of IL-1β, TNF-α, NO, MDA and DNA-binding activity of NF-κB p65 were significantly inhibited by ICT, while the activity of SOD were up-regulated at the same time.

Conclusion

ICT possessed significant neuroprotective effects in cerebral I/R mice, which might be related to prevent neuroinflammatory and oxidative damage.