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 subject...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 I h transient middle cerebral artery occlusion （MCAO） and fol- lowed by 24 h of reperfusion. Neurological deficits, infarct volume, brain edema and survive rate were measured, respectively. The levels of brain IL-1β, TNF-a, ROS and DNA-binding activity of NF-KB p65 were measured by ELISA kits. The levels of malondialdehyde （MDA） and activities of superoxide dismu- tase （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-Iβ, TNF-α, NO, MDA and DNA-binding activity of NF-KB 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.展开更多
基金financially supported by the Natural Foundation of Shandong Province (ZR2015QL002)
文摘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 I h transient middle cerebral artery occlusion （MCAO） and fol- lowed by 24 h of reperfusion. Neurological deficits, infarct volume, brain edema and survive rate were measured, respectively. The levels of brain IL-1β, TNF-a, ROS and DNA-binding activity of NF-KB p65 were measured by ELISA kits. The levels of malondialdehyde （MDA） and activities of superoxide dismu- tase （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-Iβ, TNF-α, NO, MDA and DNA-binding activity of NF-KB 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.
