ABSTRACT
Objective:To observe the effect of endurance exercise on the expression of T-cadherin, its ligand adiponectin and related downstream molecules in the myocardia of aged mice, and to explore the role of T-cadherin in the observed effects.Methods:Thirty 17-month-old C57 male mice were divided randomly into a control group and an exercise group, each of 15. Another 15 2-month-old C57 male mice constituted the young control group. The exercise group performed endurance exercises for 12 weeks, while no exercise was taken in the two control groups. All of the mice were then sacrificed within 24 hours after the exercise group′s last exercise session and the expression of T-cadherin and its ligand adiponectin was measured along with the level of phosphorylation of AMPK, apoptosis and the expression of the autophagy-related signaling proteins bax, bcl-2, Beclin-1 and p-mTOR using western blotting. Immunohistochemistry was used to observe the location and positive expression of T-cadherin, adiponectin and p-mTOR cells in the myocardium.Results:The T-cadherin was localized in the membrane and vascular endothelia of cardiomyocytes. Adiponectin was localized in the membrane, cytoplasm and vascular endothelium, and p-mTOR in the cytoplasm. Compared with the young control group, the average T-cadherin, adiponectin, AMPK activation level, apoptotic protein Bcl-2 and autophagy-promoting protein Beclin-1 expression of the aged control group was significantly lower, while the average level of the apoptotic protein bax, Caspase-9 expression, and the phosphorylation of autophagy-related protein mTOR were significantly elevated. Compared with the older control group, the average T-cadherin and ligand adiponectin, AMPK activation level, and Bcl-2 and Beclin-1 protein expression in the exercise group were significantly greater, while the average expression of bax and Caspase-9 protein was significantly lower, as was mTOR phosphorylation.Conclusions:Endurance exercise can increase the expression of T-cadherin in the myocardium, promote the binding of adiponectin to myocardial tissue, and stimulate the activation of AMPK, playing a role in protecting the myocardium, at least in elderly mice.
ABSTRACT
Objective@#To explore the effect of aerobic endurance exercise on renal fibrosis in elderly mice and its possible mechanism.@*Methods@#Thirty-six healthy, male C57 mice were sorted into a young control group (2 months old), a senile control group (19 months old) and a senile exercise group (also 19 months old). The senile exercise group underwent aerobic endurance exercise for 7 weeks. Then all of the mice were sacrificed and any changes of in their renal tissues were recorded, especially the expression of fibrosis indicators using HE staining, Sirius red staining, RT-PCRs and immunohistochemical methods.@*Results@#Collagen fibers deposited in the kidney tissue of the senile groups were significantly more numerous than in the young control group, but their number had decreased significantly after the exercise.@*Conclusion@#Aerobic endurance exercise can inhibit collagen deposition and delay the formation of renal fibrosis, at least in rats. This may be related to its inhibition of TGF-β1 and α-SMA expression and up-regulation of E-cadherin expression.