Mangiferin and Morin Attenuate Oxidative Stress, Mitochondrial Dysfunction, and Neurocytotoxicity, Induced by Amyloid Beta Oligomers
Mangiferin and morin attenuate Aβ-induced mitochondrial dyshomeostasis. (a) Aβ oligomers induce an accumulation of Ca2+ in mitochondria of neurons. Cells were transfected with the genetically encoded Ca2+ indicator 2mtD4cpv at DIV0, and [Ca2+]mit was recorded after 8–10 days in culture. Morin, but not mangiferin, reduces significantly the mitochondrial Ca2+ overload. (b) Neurons were loaded with Fluo-4 fluorescence dye and cytosolic [Ca2+] changes measured upon the addition of Aβ oligomers. Mangiferin increases the cytosolic calcium levels observed with Aβ oligomers. (A, B) Traces represent the time course of normalized average of . (c) Graphs illustrate responses of 263 (A) and 187 (B) cells from at least 5 experiments. , compared to Aβ-treated cells. (d) Morin and mangiferin attenuate mitochondrial membrane depolarization during Aβ stimulation. Cells were treated with Aβ (5 μM, 1 h) after the addition of polyphenols, and the mitochondrial membrane potential was measured using JC-1 fluorescent dye 45 min after Aβ application. Data represent normalized of the JC-1 red/green fluorescence ratio. compared with vehicle-treated cells; , compared with Aβ-treated cells. (e) Micrographs illustrate cytochrome c immunolabeling in cultured neurons after Aβ treatment (5 μM, 2 h) alone or together with morin and Mng (1 μM). Graph bars represent the intensities of cytochrome c fluorescence normalized to cell number values (, cultures) displayed as arbitrary units of fluorescence. compared with vehicle-treated cells; compared with Aβ-treated cells.
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