Secondary brain insult induced by
traumatic brain injury (TBI), including excitotoxicity, oxidative stress, inflammatory response, and neuronal degeneration, is sensitive to therapeutic interventions; therefore, searching for
neuroprotective agents represents a promising therapeutic strategy for TBI treatment.
Luteolin, a member of the
flavonoid family, has recently been proven to modulate autophagy. However, whether it activates autophagy after TBI thereby alleviating the secondary insult is not yet understood. Here, we aimed to evaluate the neuroprotection of
luteolin against TBI and the potential role of autophagy where it is involved. For this purpose, mice were randomly divided into four groups and then subjected to TBI. The treatment mice received
luteolin at a dose of 30mg/kg 30min post-TBI based on our previous study. We employed western blot, immunofluorescence and quantitative real-time PCR to determine autophagy process and inflammatory response among different groups. Autophagy was found to be enhanced after
luteolin treatment according to the expressions of autophagic markers. Furthermore,
luteolin decreased nuclear accumulation of p65 induced by TBI, indicating attenuation of
inflammation. In line with these observations,
luteolin decreased
mRNA and
protein expressions of pro-inflammatory factors IL-1b and TNF-a. At last,
luteolin reduced neuronal degeneration, and alleviated
brain edema and blood-brain barrier (BBB) disruption. In conclusion, these results implied that
luteolin protected mice brain from
traumatic brain injury by inhibiting inflammatory response, and
luteolin-induced autophagy might play a pivotal role in its neuroprotection.