摘要
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.
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.
作者
cheng-hong sun
li-hong pan
jian yang
jing-chun yao
bing-bing li
yu-jun tan
gui-min zhang
ying sun
Cheng-hong Sun , Li-hong Pan 1, Jian Yang, Jing-chun Yao, Bing-bing Li, Yu-jun Tan, Gui-min Zhanga,b, Ying Suna(a. astate Key Laboratory of Generic Manufacture Technology of Chinese Traditional Medicine, Linyi 276000, China ;b .Linyi Key Laboratory for lmmunopharmacology and lmmunotoxicology of Natural Medicine, Linyi 276000 China; c. Center for New Drug Pharrnacology. Lunnn Pharmaceutical Group corporation,Linyi 276000,chin)
基金
financially supported by the Natural Foundation of Shandong Province (ZR2015QL002)
