Protective effects of reduced dynamin-related protein 1 against amyloid beta-induced mitochondrial dysfunction and synaptic damage in Alzheimer’s disease

Icariin is a prenylated flavonol glycoside derived from the Chinese herbEpimedium sagittatumthat exerts a variety of pharmacological activities and shows promise in the treatment and prevention of Alzheimer’s disease. In this study, we investigated the neuroprotective effects of icariin against amyloid beta protein fragment 25–35 (Aβ25–35) induced neurotoxicity in cultured rat pheochromocytoma PC12 cells and explored potential underlying mechanisms. Our results showed that icariin dose-dependently increased cell viability and decreasedAβ25–35-induced apoptosis, as assessed by MTT assay and Annexin V/propidium iodide staining, respectively. Results of western blot analysis revealed that the selective phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 suppressed icariin-induced Akt phosphorylation, suggesting that the protective effects of icariin are associated with activation of the PI3K/Akt signaling pathway. LY294002 also blocked the icariin-induced downregulation of proapoptotic factors Bax and caspase-3 and upregulation of antiapoptotic factor Bcl-2 inAβ25–35-treated PC12 cells. These findings provide further evidence for the clinical efficacy of icariin in the treatment of Alzheimer’s disease.

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Protective effects of protocatechuic acid against cognitive impairment in an amyloid beta-induced Alzheimer's disease mouse model

Food and Chemical Toxicology ◽

10.1016/j.fct.2020.111571 ◽

2020 ◽

Vol 144 ◽

pp. 111571 ◽

Cited By ~ 1

Author(s):

Jung Ran Choi ◽

Ji Hyun Kim ◽

Sanghyun Lee ◽

Eun Ju Cho ◽

Hyun Young Kim

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cognitive Impairment ◽

Mouse Model ◽

Amyloid Beta ◽

Protocatechuic Acid ◽

Protective Effects

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Possible role of amyloid-beta, adenine nucleotide translocase and cyclophilin-D interaction in mitochondrial dysfunction of Alzheimer's disease

Bioinformation ◽

10.6026/97320630003440 ◽

2009 ◽

Vol 3 (10) ◽

pp. 440-445 ◽

Cited By ~ 32

Author(s):

Prabhakar Singh ◽

Shubhankar Suman ◽

Sudhir Chandna ◽

Taposh Kumar Das

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Mitochondrial Dysfunction ◽

Amyloid Beta ◽

Adenine Nucleotide ◽

Adenine Nucleotide Translocase ◽

Cyclophilin D

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Amendatory Effect of Flavonoids in Alzheimer's Disease Against Mitochondrial Dysfuntion

Current Drug Targets ◽

10.2174/1389450122666210120144921 ◽

2021 ◽

Vol 22 ◽

Author(s):

Hayrettin Ozan Gulcan ◽

Ilkay Erdogan Orhan

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Clinical Trials ◽

Drug Design ◽

Mitochondrial Dysfunction ◽

Structural Organization ◽

Protective Effects ◽

Design Studies ◽

Living Things ◽

Biological Actions

Flavonoids are chromene analogues abundantly found in plants. It is always of curiosity to discover natural flavonoid structures, since living things, including human, are routinely exposed to these compounds through many dietaries. Indeed, numerous studies conducted so far on flavonoids to display their diverse biological actions. The activity results obtained particularly on the effects of flavonoids on various validated and non-validated targets of Alzheimer’s Disease (AD) make these compounds as promising agents either to be directly employed in clinical trials or to be utilized as important scaffolds for flavonoid based drug design studies. Although there are many review articles on the treatment and protective effects of flavonoids on AD, within this review, the effects of flavonoids on mitochondrial dysfunction developing throughout AD have been presented concomitant to their structural organization.

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