Mild Traumatic Brain Injury Contributes to the Development of Delayed Neuroinflammation.

INTRODUCTION

In recent years, according to the literature, the problem of mild traumatic brain injury (mTBI) has become more and more urgent. Compared to moderate to severe craniocerebral trauma, mTBI occurs in a far greater number of people. The delayed sequelae caused by a single mTBI or multiple mTBIs are a significant public health problem.

METHODS

A weight-drop model was used for the formation of mTBI. A metal rod weighing 337 g with a blunt tip of 3 mm diameter was uplifted at 8 cm height and held by a lever. The trauma was created by lowering the lever and the rod and free-dropping onto the rat skull. In the cerebral cortex of experimental animals, we analyzed the level of microglial activity (Iba-1-positive system) and the expression of pro-inflammatory markers (IL1β, IL6, and CD86). Also, the expression level of the endocannabinoid system receptor (cannabinoid receptor type 1 [CB1]) was assessed in brain samples.

RESULTS

Experiments have shown that mTBI increases (1) the amount of microglia (iba-1) activated by the pro-inflammatory pathway (CD86); (2) the level of pro-inflammatory cytokines IL1β and IL6; and (3) CB1R activity.

CONCLUSION

Overall, the results of this study indicate that mTBI induces a sustained neuroinflammatory response.