Amyloid beta（Aβ）-induced oxidative stress is a major pathologic hallmark of Alzheimer＇s disease. Cyanidin, a natural flavonoid compound, is neuroprotective against oxidative damage-mediated degeneration. However, ...Amyloid beta（Aβ）-induced oxidative stress is a major pathologic hallmark of Alzheimer＇s disease. Cyanidin, a natural flavonoid compound, is neuroprotective against oxidative damage-mediated degeneration. However, its molecular mechanism remains unclear. Here, we investigated the effects of cyanidin pretreatment against Aβ-induced neurotoxicity in PC12 cells, and explored the underlying mechanisms. Cyanidin pretreatment significantly attenuated Aβ-induced cell mortality and morphological changes in PC12 cells. Mechanistically, cyanidin effectively blocked apoptosis induced by Aβ, by restoring the mitochondrial membrane potential via upregulation of Bcl-2 protein expression. Moreover, cyanidin markedly protected PC12 cells from Aβ-induced DNA damage by blocking reactive oxide species and superoxide accumulation. These results provide evidence that cyanidin suppresses Aβ-induced cytotoxicity, by preventing oxidative damage mediated by reactive oxide species, which in turn inhibits mitochondrial apoptosis. Our study demonstrates the therapeutic potential of cyanidin in the prevention of oxidative stress-mediated Aβ neurotoxicity.展开更多
Dear Editor,Parkinson’s disease (PD) is the second most common neurodegenerative disease in the elderly (1, 2)PD affects1%–2%of the world’s population older than 65 years(3–5)In recent years, large-scale genome-wi...Dear Editor,Parkinson’s disease (PD) is the second most common neurodegenerative disease in the elderly (1, 2)PD affects1%–2%of the world’s population older than 65 years(3–5)In recent years, large-scale genome-wide association studies (GWAS) have been widely conducted to identify the common genetic risk genes for PD. A number of PD susceptibility genes have been identified, including SNCA,MAPT, NUCKS1, the HLA region, GAK, BST1, GBA,WNT3, RIT2, and LRRK2 [3–5].展开更多
基金supported by the Natural Science Foundation of Shandong Province of China,No.ZR2014HM046(to ZCZ)
文摘Amyloid beta（Aβ）-induced oxidative stress is a major pathologic hallmark of Alzheimer＇s disease. Cyanidin, a natural flavonoid compound, is neuroprotective against oxidative damage-mediated degeneration. However, its molecular mechanism remains unclear. Here, we investigated the effects of cyanidin pretreatment against Aβ-induced neurotoxicity in PC12 cells, and explored the underlying mechanisms. Cyanidin pretreatment significantly attenuated Aβ-induced cell mortality and morphological changes in PC12 cells. Mechanistically, cyanidin effectively blocked apoptosis induced by Aβ, by restoring the mitochondrial membrane potential via upregulation of Bcl-2 protein expression. Moreover, cyanidin markedly protected PC12 cells from Aβ-induced DNA damage by blocking reactive oxide species and superoxide accumulation. These results provide evidence that cyanidin suppresses Aβ-induced cytotoxicity, by preventing oxidative damage mediated by reactive oxide species, which in turn inhibits mitochondrial apoptosis. Our study demonstrates the therapeutic potential of cyanidin in the prevention of oxidative stress-mediated Aβ neurotoxicity.
基金supported in part by the National Natural Science Foundation of China (81471212)the Taishan Scholar Project to BLS
文摘Dear Editor,Parkinson’s disease (PD) is the second most common neurodegenerative disease in the elderly (1, 2)PD affects1%–2%of the world’s population older than 65 years(3–5)In recent years, large-scale genome-wide association studies (GWAS) have been widely conducted to identify the common genetic risk genes for PD. A number of PD susceptibility genes have been identified, including SNCA,MAPT, NUCKS1, the HLA region, GAK, BST1, GBA,WNT3, RIT2, and LRRK2 [3–5].
