Attenuation of neurological injury with early baicalein treatment following subarachnoid hemorrhage in rats

Abstract

ObjectBaicalein has been shown to offer neuroprotection in the ischemic brain, but its effect in subarachnoid hemorrhage (SAH) is unknown. The authors used a double-hemorrhage model to study the role of early baicalein treatment in SAH.MethodsSubarachnoid hemorrhage was induced in male Wistar rats through a repeat injection of autologous blood at a 48-hour interval. Rats subjected or not subjected to SAH received a 30-mg/kg baicalein injection 3 hours after SAH and daily for 6 consecutive days, and results were compared with those obtained in vehicle-treated control rats. Mortality of the rats was recorded. Neurological outcome was assessed daily. Cerebrospinal fluid dialysates were collected and examined for glutamate concentrations. Cerebral vasospasm (CVS), brain water content, neuron variability, expression of glutamate transporter–1 (GLT-1), immunoreactivity of astrocyte, and level of malondialdehyde, activities of superoxide dismutase (SOD), and catalase in brain tissues content were determined on post-SAH Day 7.ResultsMortality rate, neuronal degeneration, brain water content, and CVS were decreased and neurological function improved in the baicalein-treated rats. Baicalein increased astrocyte activity and preserved GLT-1, which attenuated the glutamate surge after SAH. Baicalein also provided antioxidative stress by preserving activities of SOD and catalase and decreased malondialdehydelevel after SAH. The glutamate, body weight, neurological scores, and glial fibrillary acidic protein activity were significantly correlated. The CVS was correlated with neuronal degeneration, and GLT-1 was correlated with oxidative stress.ConclusionsEarly baicalein treatment attenuated CVS and limited neurological injury following SAH. These data may indicate clinical utility for baicalein as an adjunct therapy to reduce brain injury and improve patient outcomes.

Progesterone alleviates acute brain injury via reducing apoptosis and oxidative stress in a rat experimental subarachnoid hemorrhage model

“…Acute brain injury after SAH is emerging as the main cause of the poor prognosis after SAH. Many studies have demonstrated that alleviating acute brain injury after SAH via various pathways may effectively mitigate the neural damage caused by SAH [17]. Several studies have shown the neuroprotective effects of PROG in numerous animal injury models, including traumatic brain injury, spinal cord injury, and ischemic stroke [18][19][20].…”

Neuroprotective Effect of Hydrogen-Rich Saline against Neurologic Damage and Apoptosis in Early Brain Injury following Subarachnoid Hemorrhage: Possible Role of the Akt/GSK3β Signaling Pathway

“…According to literature, the main cause of oxidative stress following SAH is oxyhaemoglobin release from erythrocytes in the subarachnoid blood clot [33], [34]. The increased level of oxidative stress, which occurs in different brain cells including neurons, is accompanied by neuronal apoptosis after SAH [8], [35], [36]. Therefore, inhibiting oxidative stress-induced neuronal apoptosis is a critical intervention strategy in SAH, and a line of evidence demonstrated that many antioxidant treatment reduced apoptosis of neurons after SAH [13], [16], [29].…”

Hydrogen-Rich Saline Attenuated Subarachnoid Hemorrhage-Induced Early Brain Injury in Rats by Suppressing Inflammatory Response: Possible Involvement of NF-κB Pathway and NLRP3 Inflammasome

“…It is widely accepted that free radicals generation and intrinsic antioxidant enzyme system deficiency both contribute to oxidative stress, followed by the inflammatory and cellular injury response in SAH [8,10,11,17,18]. In line with this, research concerning free radicals scavenge has shown that anti-oxidative agents may improve the outcome of SAH patients [19][20][21]. Therefore, anti-oxidative treatment using free radical scavengers has been supposed a promising treatment strategy in SAH patients.…”