Department of Anesthesiology.
J Neurosurg. 2013 Oct;119(4):1028-37. doi: 10.3171/2013.4.JNS121919. Epub 2013 May 31.
Baicalein 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.
Subarachnoid 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.
Mortality 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.
Early 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.
黄芩素已被证明可在缺血性大脑中提供神经保护，但在蛛网膜下腔出血（SAH）中的作用尚不清楚。作者使用双重出血模型来研究早期黄芩素治疗在 SAH 中的作用。
通过在 48 小时间隔内重复注射自体血液，在雄性 Wistar 大鼠中诱导蛛网膜下腔出血。接受或不接受 SAH 的大鼠在 SAH 后 3 小时接受 30mg/kg 黄芩素注射，并连续 6 天每天接受一次，结果与接受载体处理的对照大鼠进行比较。记录大鼠死亡率。每日评估神经功能。收集脑脊液透析液并检查谷氨酸浓度。在 SAH 后第 7 天测定脑血管痉挛（CVS）、脑水含量、神经元变异性、谷氨酸转运体-1（GLT-1）的表达、星形胶质细胞的免疫反应性和脑组织中丙二醛的水平、超氧化物歧化酶（SOD）和过氧化氢酶的活性。
黄芩素治疗组大鼠死亡率、神经元变性、脑水含量和 CVS 降低，神经功能改善。黄芩素增加了星形胶质细胞的活性并保留了 GLT-1，从而减轻了 SAH 后的谷氨酸激增。黄芩素还通过保存 SOD 和过氧化氢酶的活性以及降低 SAH 后的丙二醛水平提供了抗氧化应激作用。谷氨酸、体重、神经评分和胶质纤维酸性蛋白活性显著相关。CVS 与神经元变性相关，GLT-1 与氧化应激相关。
早期黄芩素治疗可减轻 SAH 后的 CVS 和神经损伤。这些数据可能表明黄芩素作为辅助治疗减轻脑损伤和改善患者预后的临床应用。
