Troxerutin cerebroprotein hydrolysate injection ameliorates neurovascular injury induced by traumatic brain injury - via endothelial nitric oxide synthase pathway regulation.
Mots clés
Abstrait
BACKGROUND
Neurovascular dysfunction caused by traumatic brain injury (TBI) is characterized by cerebralvascular damage, blood-brain barrier (BBB) breakdown, brain edema, etc. This study was designed to assess the protective role of 5 days troxerutin cerebroprotein hydrolysate (TCH) injection treatment against TBI, as well as the potential mechanism.
METHODS
The weight-drop model of TBI in male Sprague-Dawley rats was chosen to induce TBI model, rats either with TCH or a vehicle via intraperitoneal injection were examined 3 days after TBI.
RESULTS
TCH resulted in alleviation of neurological deficits, reduction of infarct volume, improvement of regional cerebral blood flow (rCBF), amelioration of neuronal death, astrocyte proliferation, endothelial cell loss, and BBB dysintegrity. These effects of TCH treatment against TBI were through endothelial nitric oxide synthase (eNOS) coupling/decoupling status adjustment, which not only increased nitric oxide (NO) level, but also decreased peroxynitrate level expression.
CONCLUSIONS
All the results indicated that TCH injection has multifaceted protective effects of neurovascular unit (NVU) against TBI via eNOS pathway regulation.
