Digitoflavone provokes mitochondrial biogenesis in PC12 cells: A protective approach to oxidative stress.

Pharm Biol 2015 9;53(12):1727-34. Epub 2015 Apr 9.

NeuroBiology Research Center and.

Context: Reactive oxygen species (ROS) are known to be one of the main causes of neurodegenerative disorders, and flavonoids play characteristic roles in a variety of biological activities, and specially are known to be antioxidant reagents.

Objective: In this study, we investigated neuroprotective effects of digitoflavone to suppress H2O2 -induced cell death in neuron-like PC12 cells.

Material And Methods: PC12 cells were pre-treated with digitoflavone for 2 h and then cells were exposed to H2O2 for 18 h. The cells' viability was evaluated by MTT assay. Rhodamine 123 staining was used for the determination of mitochondrial membrane potential (ΔΨm). The intracellular ROS aggregation was determined by using 2',7'-dichlorofluorescein diacetate. Also, the level of mitochondrial biogenesis factors was measured by western blot. The antioxidant capacity of digitoflavone was also determined by measuring reduced glutathione (GSH) level and catalase (CAT) activity quantification.

Results: Digitoflavone significantly elevated cells' viability at concentrations of 10 and 20 µM. Also, digitoflavone attenuated intracellular level of ROS, and stabilized ΔΨm. Moreover, digitoflavone increased phosphorylation of AMP-activated protein kinase (AMPK) and, consequently, elevated mitochondrial biogenesis factors which were reduced after H2O2 exposure. We emphasized on the protective effect of digitoflavone through increasing mitochondrial biogenesis by specifically inhibiting AMPK. Antioxidant ability of digitoflavone was indicated by the elevation of GSH level and CAT activity.

Conclusion: As a result, digitoflavone stabilize ΔΨm, enhanced cell viability through inducing mitochondrial biogenesis pathway, and increased antioxidant capacity of the cells which lead to better combating the oxidative stress.

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Source
http://www.tandfonline.com/doi/full/10.3109/13880209.2015.10
Publisher Site
http://dx.doi.org/10.3109/13880209.2015.1005749DOI Listing
May 2016

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