| Status | 已發表Published |
| Artemether confers neuroprotection on Alzheimer's disease through stimulation of the AMPK /GSK3β(ser9)/ Nrf2 signaling pathway | |
Li , S.; Zheng, W. 
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| 2021-07-01 | |
| Source Publication | 7th macau symposium on Biomedical Science
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| Abstract | Objective: Alzheimer's disease is a progressive neurodegenerative disease and the most common cause of senile dementia. Although the cause of AD is still unclear, increasing evidences indicate that excessive reactive oxygen species (ROS) impairing the physiological functions may be an underlying mechanism of this disease. Therefore, drugs that can effectively protect neuronal cells from oxidative damage holds potential for treating and slowing down the process of AD. Methods: Aβ1-42 induced neurotoxicity and the protective effect of artemether in neuronal cultures was measured by MTT and LDH assay. Apoptosis was measured by Hoechst 33342 assay, caspase activity and fluorescence-activated cell sorter of Annexin-V-FITC labeled neurons. Oxidative stress was followed up by measurements of intracellular reactive oxygen species and mitochondrial membrane potential. The phosphorylation of signaling proteins was measured by western blotting. Mice memory was evaluated by Morris water maze test. Brain cortical apoptosis was performed by TUNEL assay. Oxidative stress was determined by lipid peroxidation and superoxide dismutase activity measurements. Aβ expression and tau proteins phosphorylation was determined by Immunohistochemistry. Results: Pre-treatment with artemether attenuated neurotoxicity induced by Aβ1-42 in different neuronal cell cultures. A temporal correlation was found between artemether neuroprotection towards Aβ-induced neurotoxicity and the activation of AMPK/GSK3β and Nrf2 signaling. In 3xTg-AD mice, artemether therapy attenuated spatial learning and reference memory, inhibited brain neuronal apoptosis and glial activation, inhibited oxidative stress by decreasing lipid peroxidation and increasing SOD activity, reduced Aβ deposition and tau phosphorylation and activated AMPK/GSK3β and Nrf2 signaling. Conclusion: These findings suggest that artemether produced neuroprotective effects in neuronal cultures and 3xTg-AD mice which might be responsible for the neurotherapeutic effects. Artemether is proposed as a new drug for the prevention and treatment of AD disease. |
| Keyword | Alzheimer's disease artemether AMPK /GSK3β(ser9)/ Nrf2 |
| Language | 英語English |
| The Source to Article | PB_Publication |
| PUB ID | 57988 |
| Document Type | Conference paper |
| Collection | DEPARTMENT OF PHARMACEUTICAL SCIENCES |
| Corresponding Author | Zheng, W. |
| Recommended Citation GB/T 7714 | Li , S.,Zheng, W.. Artemether confers neuroprotection on Alzheimer's disease through stimulation of the AMPK /GSK3β(ser9)/ Nrf2 signaling pathway[C], 2021. |
| APA | Li , S.., & Zheng, W. (2021). Artemether confers neuroprotection on Alzheimer's disease through stimulation of the AMPK /GSK3β(ser9)/ Nrf2 signaling pathway. 7th macau symposium on Biomedical Science. |
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