Nicotinamide adenine dinucleotide alleviates neuroinflammation in rats with traumatic brain injury.

OBJECTIVE

To characterize the pathology and pathophysiological processes within 6 h after Traumatic brain injury (TBI) in rats, elucidate the neuroprotective effects and the underlying mechanisms of Nicotinamide Adenine Dinucleotide (NAD) in the early stage of TBI to explore the feasibility and clinical benefits of applying NAD directly to the localized injury after TBI.

MATERIAL AND

METHODS

54 male Sprague-Dawley (SD) rats aged 6-8 weeks were randomly assigned equally to three groups, sham-operated surgery (SO) with saline treatment (SO + Saline), TBI with saline treatment (TBI + Saline), and TBI with 10 μM NAD treatment (TBI + NAD). The whole brain tissues were collected at 1, 3, and 6 h following the procedure. Levels of biomarkers for TBI including S100β, TNF-α, occludin, PPARβ/δ were measured.

RESULTS

Significant neuroinflammation was observed in the rat brains after TBI, which peaked at 3 h following injury. Significant changes in S100β, TNF-α, PPARβ/δ, and occluding were also observed. Treatment with NAD significantly alleviated neuroinflammation at 1 h following TBI.

CONCLUSIONS

TBI caused severe neuroinflammation in rat brains, which peaked at 3 h following injury. Treatment with NAD alleviated neuroinflammation in TBI rats.