Oxidative stress, owing to the excessive production of ROS （reactive oxygen species）, is one of the leading causes for the progression of AD （Alzheimer＇s disease）. Increasing evidences suggested that oxidative st...Oxidative stress, owing to the excessive production of ROS （reactive oxygen species）, is one of the leading causes for the progression of AD （Alzheimer＇s disease）. Increasing evidences suggested that oxidative stress insult impaired the physiological functioning of neuronal cells by inducing cell apoptosis. The search for drug candidates that can effectively protect neurons from oxidative stress insult might hold therapeutic potential for AD. In the present study, we tested the neuroprotective effects and the related action mechanisms of artemisinin, a FDA-approved anti-malarial drug, against H2O2 induced oxidative damage in PC12 cells. It was found that artemisinin reduced cell viability loss caused by hydrogen peroxide （H2O2） in PC12 cells. In addition, data from Flow cytometry displayed that artemisinin significantly decreased the apoptosis of PC 12 cells induced by H2O2. Furthermore Western blot analysis displayed that artemisinin stimulated the p38MAPK signaling, while treatment of PC 12 cells with specific p38MAPK pathway inhibitor SB203580 blocked the neuroprotective effect of artemisinin. These results together indicated that artemisinin is a potential protectant, and it protects PC12 cells against H2O2 injury through activation of the p38MAPK pathway.展开更多
基金Acknowledgements This research was financially supported by the National Natural Science Foundation of China （31371088） the Guangdong Provincial Project of Science and Technology （2011B050200005） SRG2015-00004-FHS and MYRG2016-00052-FHS from University of Macao, and the Science and Technology Development Fund （FDCT） of Macao （FDCT 021/2015/A1 and FDCT016/2016/A1）.
文摘Oxidative stress, owing to the excessive production of ROS （reactive oxygen species）, is one of the leading causes for the progression of AD （Alzheimer＇s disease）. Increasing evidences suggested that oxidative stress insult impaired the physiological functioning of neuronal cells by inducing cell apoptosis. The search for drug candidates that can effectively protect neurons from oxidative stress insult might hold therapeutic potential for AD. In the present study, we tested the neuroprotective effects and the related action mechanisms of artemisinin, a FDA-approved anti-malarial drug, against H2O2 induced oxidative damage in PC12 cells. It was found that artemisinin reduced cell viability loss caused by hydrogen peroxide （H2O2） in PC12 cells. In addition, data from Flow cytometry displayed that artemisinin significantly decreased the apoptosis of PC 12 cells induced by H2O2. Furthermore Western blot analysis displayed that artemisinin stimulated the p38MAPK signaling, while treatment of PC 12 cells with specific p38MAPK pathway inhibitor SB203580 blocked the neuroprotective effect of artemisinin. These results together indicated that artemisinin is a potential protectant, and it protects PC12 cells against H2O2 injury through activation of the p38MAPK pathway.
