Alterations in expression of α1-adrenergic receptors possibly are involved in prevention of age-associated apoptosis in rat hippocampus by treadmill exercise
Author:
Chodari Leila12, Ghasemi Maedeh3, Mehranfard Nasrin1ORCID
Affiliation:
1. Neurophysiology Research Center , Cellular and Molecular Medicine Research Institute, Urmia University of Medical Sciences , Urmia , Iran 2. Department of Physiology , Faculty of Medicine, Urmia University of Medical Sciences , Urmia , Iran 3. Department of Physiology , School of Medicine, Isfahan University of Medical Sciences , Isfahan , Iran
Abstract
Abstract
Objectives
Exercise is assumed to attenuate age-related neuronal apoptosis, but the detailed mechanism(s) is not fully understood. α1-Adrenergic receptors (ARs) can either trigger or suppress apoptosis, therefore, here we determined the impact of treadmill exercise on the expression of the apoptosis regulatory proteins as well as α1-AR subtypes α1A- and α1B-ARs, in order to elucidate a possible association between apoptosis and the hippocampal expression of α1-ARs in aged male rats.
Methods
Twenty-one male Wistar rats were divided into 3 groups (n=7): young control, aged sedentary, and aged + exercise. Western blot for α1A- and α1B-ARs as well as pro-(Bax and p53) and anti-apoptotic (Bcl2) proteins was conducted. An 8-week regular moderate-intensity treadmill exercise intervention was carried out in exercise group.
Results
In aged rats, α1A-AR expression in the hippocampus was significantly increased, and exercise markedly prevented this event. While α1B-AR expression was no altered with aging, a marked reduction in α1B-AR level was detected in exercise group when compared to aged group. Furthermore, pro-apoptotic protein levels of Bax and p53 were upregulated and anti-apoptotic protein Bcl2 was downregulated in the aging hippocampus, but could be reversed by treadmill exercise. In the present research, exercise-induced reduction in α1A- and α1B-ARs was associated with an obvious downregulation of Bax/Bcl2 ratio in aged rats, suggesting that exercise may inhibit apoptosis through regulating α1-ARs, particularly α1A-AR.
Conclusions
Our study suggests that manipulations attenuating α1-AR activity, including nonselective α1-adrenergic antagonists, may protect against hippocampal neurodegeneration in aging brains.
Funder
Neurophysiology Research Center, Cellular and Molecular Medicine Research Institute, Urmia University of Medical Sciences
Publisher
Walter de Gruyter GmbH
Subject
Complementary and alternative medicine
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