Mangiferin and Morin Attenuate Oxidative Stress, Mitochondrial Dysfunction, and Neurocytotoxicity, Induced by Amyloid Beta Oligomers
Aβ-induced respiratory inhibition is rescued by morin and mangiferin. (a) Primary neurons in the presence or absence of morin or mangiferin (1 μM) were exposed to vehicle or Aβ (5 μM, 1 h) in XF Base medium (Seahorse Bioscience) containing 1 mM pyruvate, 2 mM glutamine, and 10 mM glucose, and mitochondrial oxygen consumption rate (OCR) was measured using a extracellular flux analyzer (Seahorse XFe96 analyzer). Mitochondrial function in neurons was determined through sequential addition of 2 μM oligomycin, 1 μM FCCP, and rotenone plus antimycin A (both 0.5 μM). This allowed the determination of basal oxygen consumption (BR), oxygen consumption linked to ATP synthesis (ATP) and mitochondrial uncoupled respiration (MUR) (see methods for OCR calculation). (b) Aβ oligomers caused mitochondrial dysfunction. Graph bars represent the of BR, ATP, and MUR OCR in vehicle-treated cells (37 ± 2.5, 25.3 ± 1.5 and 45.4 ± 1.8 pmol/min) versus Aβ-treated cells (31 ± 2, 21 ± 1.5 and 35.2 ± 3 pmol/min), respectively. , cultures. (c) Morin and Mng rescued the Aβ-induced mitochondrial respiration inhibition. Graph bars represent the average ± SEM of BR, ATP, and MUR OCR in Aβ-treated, Aβ + morin-treated, and Aβ + Mng-treated cells. , comparing antioxidant-treated cells with Aβ-treated cells. (d) Morin and Mng treatments did not change significantly the OCR in any parameters of mitochondrial respiration BR, ATP, and MUR (n.s.: not significant).
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