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Astaxanthin protects against kainic acid-induced seizures and pathological consequences
Neurochemistry international ( IF 4.2 ) Pub Date : 2018-02-21 , DOI: 10.1016/j.neuint.2018.02.008
Yi Chang , Cheng Wei Lu , Yi Jing Chen , Tzu Yu Lin , Shu Kuei Huang , Su Jane Wang

Excitotoxic damage caused by increased glutamate levels is involved in the pathogenesis of neurodegenerative diseases. Astaxanthin, a natural carotenoid with multiple health benefits, inhibits glutamate release from the brain tissue; however, whether it possesses the ability to affect glutamate-induced brain injury is unknown. The present study investigated the neuroprotective effects of astaxanthin on kainic acid (KA)-induced excitotoxicity in rats and the possible underlying intracellular signaling pathway. The rats were orally administrated with astaxanthin (50 or 100 mg/kg) for 7 days (once a day), and KA (15 mg/kg) was administered intraperitoneally at 1 h after the final administration. The results revealed that KA induced seizures, increased the hippocampal glutamate levels, caused considerable neuronal death and microglial activation in the hippocampal CA3 regions, and increased the production of proinflammatory cytokines. Astaxanthin pretreatment prevented these changes. Furthermore, astaxanthin pretreatment increased the expression of neuronal cell survival-related factors, including phosphorylated Akt, phosphorylated glycogen synthase kinase-3β, and Bcl-2 in the hippocampus of KA-injected rats. These results suggested that astaxanthin can attenuate seizures, mitigate inflammation, augment survival signals, and prevent hippocampal neuronal damage in the animal model of KA-induced excitotoxicity.



中文翻译:

虾青素可防止海藻酸引起的癫痫发作和病理后果

谷氨酸水平升高引起的兴奋性毒性损害与神经退行性疾病的发病机理有关。虾青素是一种具有多种健康益处的天然类胡萝卜素,可抑制谷氨酸从脑组织中释放出来。但是,它是否具有影响谷氨酸诱导的脑损伤的能力尚不清楚。本研究调查了虾青素对海藻酸(KA)诱导的大鼠兴奋性中毒的神经保护作用以及可能的潜在细胞内信号传导途径。给大鼠口服虾青素(50或100 mg / kg)7天(每天一次),最后一次给药后1 h腹膜内给予KA(15 mg / kg)。结果显示,KA诱发癫痫发作,增加了海马谷氨酸水平,引起海马CA3区大量神经元死亡和小胶质细胞活化,并增加促炎细胞因子的产生。虾青素预处理可防止这些变化。此外,虾青素预处理可增加神经元细胞存活相关因子的表达,包括磷酸化的Akt,磷酸化的糖原合酶激酶3β和Bcl-2在注射KA的大鼠海马中的表达。这些结果表明,在KA诱导的兴奋性毒性动物模型中,虾青素可以减轻癫痫发作,减轻炎症,增强生存信号并防止海马神经元损伤。虾青素预处理可增加神经元细胞存活相关因子的表达,其中包括磷酸化的Akt,磷酸化的糖原合酶激酶3β和Bcl-2在注射KA的大鼠海马中。这些结果表明,在KA诱导的兴奋性毒性动物模型中,虾青素可以减轻癫痫发作,减轻炎症,增强生存信号并防止海马神经元损伤。虾青素预处理可增加神经元细胞存活相关因子的表达,其中包括磷酸化的Akt,磷酸化的糖原合酶激酶3β和Bcl-2在注射KA的大鼠海马中。这些结果表明,在KA诱导的兴奋性毒性动物模型中,虾青素可以减轻癫痫发作,减轻炎症,增强生存信号并防止海马神经元损伤。

更新日期:2018-02-21
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