Exercise training improves age-related changes in cerebral capillary vascularity through the upregulation of PI3K / Akt signaling

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Channipa Chanpakdee
Sheepsumon Viboolvorakul
Suthiluk Patumraj


Background: Currently, the number of the elderly has been rising sharply worldwide. Seemingly, age-induced
cerebral endothelial dysfunction may lead to vascular abnormality that can later progress to cerebrovascular
and neurodegenerative diseases. Moreover, several evidences have shown that age-related oxidative stress and
decline in cellular function appeared in the vascular system both in humans and laboratory animals. The role of
exercise training in the regulation of age-related oxidative stress and endothelial functions have been reported.

Objectives: To investigate whether exercise training can prevent age-induced cerebral endothelial dysfunction
associated to PI3K/Akt signaling.

Methods: Male Wistar rats were randomly divided into 3 groups: sedentary-young group (SE-Young, 4 months),
sedentary-aged group (SE-Aged, 22 - 24 months), and swimming trained-aged group (ET-Aged, 22 - 24 months),
which individually swam 1 hour/day, 5 days/week for 8 weeks. After 8 weeks of the exercise period, the rats took
rest for 24 hours. After a phosphate buffer saline (PBS) perfusion, brain was used for determining CD31 by
immunohistochemistry. Vascular endothelial growth factor (VEGF), phospho-Akt level (p-Akt), and malondialdehyde (MDA) levels in the brain were measured by enzyme-linked immunosorbent assay.

Results: The aged rats’ physiological characteristics had significant alteration when compared to the young
group (P < 0.05). However, ET-Aged rats showed significantly reduced resting mean arterial blood pressure when
compared to the young group (P < 0.05). This study also showed that exercise could upregulate VEGF, p-Akt level, and increase CD31 in the ET-aged group. Furthermore, tissue MDA in ET-Aged rats was significantly reduced when compared to SE-Aged rats (P < 0.05).

Conclusion: Our findings imply that exercise training protected age-induced cerebral endothelial dysfunction
associated with its effects of oxidative stress and PI3K/Akt signaling.

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