Effect of Gastrodin on Early Brain Injury and Neurological Outcome After Subarachnoid Hemorrhage in Rats
Male
Neurons
Brain
Glutamic Acid
Apoptosis
Brain Edema
Subarachnoid Hemorrhage
3. Good health
Rats, Sprague-Dawley
Oxidative Stress
03 medical and health sciences
Neuroprotective Agents
0302 clinical medicine
Glucosides
Blood-Brain Barrier
Astrocytes
Animals
Calcium
Microglia
Benzyl Alcohols
DOI:
10.1007/s12264-018-00333-w
Publication Date:
2019-01-24T15:37:57Z
AUTHORS (7)
ABSTRACT
Gastrodin is a phenolic glycoside that has been demonstrated to provide neuroprotection in preclinical models of central nervous system disease, but its effect in subarachnoid hemorrhage (SAH) remains unclear. In this study, we showed that intraperitoneal administration of gastrodin (100 mg/kg per day) significantly attenuated the SAH-induced neurological deficit, brain edema, and increased blood-brain barrier permeability in rats. Meanwhile, gastrodin treatment significantly reduced the SAH-induced elevation of glutamate concentration in the cerebrospinal fluid and the intracellular Ca2+ overload. Moreover, gastrodin suppressed the SAH-induced microglial activation, astrocyte activation, and neuronal apoptosis. Mechanistically, gastrodin significantly reduced the oxidative stress and inflammatory response, up-regulated the expression of nuclear factor erythroid 2-related factor 2, heme oxygenase-1, phospho-Akt and B-cell lymphoma 2, and down-regulated the expression of BCL2-associated X protein and cleaved caspase-3. Our results suggested that the administration of gastrodin provides neuroprotection against early brain injury after experimental SAH.
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