The effect of fibroblast growth factor 21 on a cellular model of Alzheimerייs disease with emphasis on cell viability and mitochondrial membrane potential

Background and Objective: Alzheimer’s disease (AD) is a neurodegenerative disorder which is associated with extracellular accumulation of amyloid beta (AB) plaques. AD is accompanied by mitochondrial dysfunction and energy metabolism reduction. Fibroblast growth factor 21 (FGF21) is an endogenous polypeptide which its beneficial effects have been demonstrated on mitochondrial function, energy metabolism regulation and neuroprotection. Materials and Methods: The present study was performed to investigate the effect of pretreatment with different concentrations of FGF21 [100,200 and 400 nM] on SH-SY5Y cells as a cellular model of AD induced by A(beta)(1-42). For induction of cellular model of AD. A(beta)(1-42) [20 µM] was added to SH-SY5Y cell medium. Cell viability (MTT assay) and mitochondrial membrane potential changes (Rhodamine 123 fluorescence intensity) were measured using microplate reader. Results: The results of this study showed that A(beta)(1-42) enhances cell damage (p < 0.05) and decreases mitochondrial membrane potential (p < 0.05). Pretreatment of SH-SY5Y cells with FGF21 increased cell viability (p < 0.05- 0.001) and mitochondrial membrane potential (p < 0.05-0.01) in a concentration-dependent manner. Conclusion: Taken together, the results of this study suggest that FGF21 prevents cell death induced by A(beta)(1-42) in SH-SY5Y cells. It seems that the beneficial effects of FGF21 are mediated through mitochondrial membrane potential maintenance.