MicroRNAs (miRNAs) have been reported to be involved in many neurodegenerative diseases. In order to explore the regulatory role of miR-34a in aging-related diseases such as Alzheimer's disease (AD) during exercise intervention, we constructed a rat model with (D-galactose) D-gal-induced oxidative stress and cognitive impairment coupled with dysfunctional autophagy and abnormal mitochondrial dynamics, determined the mitigation of cognitive impairment of D-gal-induced aging rats during swimming intervention, and evaluated miR-34a-mediated functional status of autophagy and abnormal mitochondrial dynamics. Meanwhile, whether the up-regulation of miR-34a can lead to dysfunctional autophagy and abnormal mitochondrial dynamics was confirmed in human SH-SY5Y cells with silenced miR-34a by the transfection of miR-34a inhibitor. Results indicated that swimming intervention could significantly attenuate cognitive impairment, rescue the up-regulation of miR-34a, mitigate the dysfunctional autophagy, and inhibit the increase of Drp1 in D-gal-induced aging model rats. In contrast, miR-34a inhibitor in cell model not only attenuated D-gal-induced autophagy impairment, but also decreased the expression of Drp1 and Mfn2. Therefore, swimming training can attenuate the impairment of miR-34a-mediated autophagy and abnormal mitochondrial dynamics during D-gal-induced aging process in rat hippocampal tissue, which may be one of the mechanisms for delaying brain aging through swimming training, and miR-34a could be the novel therapeutic target for aging-related diseases such as AD.
- swimming training
- mitochondrial dynamics
- Copyright © 2017, Journal of Applied Physiology