Protective effects of early exercise on neuroinflammation, and neurotoxicity associated by traumatic brain injury: a behavioral and neurochemical approach

Abstract

Objective

The benefits of exercise in TBI have been proven. However, the time-dependent effects of exercise initiation and the involved mechanisms are controversial. We investigated the effects of preconditioning, continuous, early, and delayed treadmill exercise on motor behavior, brain edema, inflammation, and oxidative stress in experimental traumatic brain injury (TBI).

Materials and Methods

48 male rats were assigned into two groups: sedentary control (Sham and TBI) and exercise groups: 1MB (preconditioning, initiation beginning at 1 month before trauma), 1MBA (continuous, initiation beginning at 1 month before and continuing 1 month after trauma), 24hA (early, initiation beginning at 24 h after trauma), and 1WA (delay, initiation beginning at 1 week after trauma). The rats in exercise groups were forced to run on a treadmill five days a week for 30 min per day. Rotarod and open file were used to assess motor behavior. ELISA was also used to measure total antioxidant capacity (TAC), tumor necrosis factor-alpha (TNF-α), and malondialdehyde (MDA) in serum and CSF.

Results

Exercise significantly decreased neurological impairments, motor deficits, and apoptosis compared with the sedentary group. Early (within 24 h) and ongoing (1 MBA) exercise significantly improved motor behavior after TBI. In addition, these exercise programs inhibited brain edema and the number of apoptotic cells. MDA and TNF-α levels increased in all exercise groups, but the effects were greater after early exercise than after delayed exercise, resulting in a significant decrease in TAC levels in serum and CSF. We discovered a positive correlation between MDA, TAC, and TNF-α concentration in serum and CSF.

Conclusion

Our finding suggests that early exercise (24hA) and 1MBA groups afford neuroprotection and reduce the second injury consequence, probably by reducing neuronal apoptosis and oxidative stress.

Keywords:

• Brain injury
• malondialdehyde
• apoptosis
• oxidative stress
• inflammation
• motor behavior
• brain edema
• MDA
• TAC

Disclosure statement

No potential conflict of interest was reported by the authors.

Data availability statement

Data will be made available on reasonable request.

Table 1. The changes of histopathological factors in Cortex.

Funding

The author(s) reported there is no funding associated with the work featured in this article.