...
首页> 外文期刊>Protoplasma: An International Journal of Cell Biology >Attenuation of oxidative damage-associated cognitive decline by Withania somnifera in rat model of streptozotocin-induced cognitive impairment
【24h】

Attenuation of oxidative damage-associated cognitive decline by Withania somnifera in rat model of streptozotocin-induced cognitive impairment

机译:WithWithania somnifera在链脲佐菌素诱发的认知障碍大鼠模型中对氧化损伤相关的认知能力下降的减弱

获取原文
获取原文并翻译 | 示例
           

摘要

Oxidative stress is a critical contributing factor to age-related neurodegenerative disorders. Therefore, the inhibition of oxidative damage, responsible for chronic detrimental neurodegeneration, is an important strategy for neuroprotective therapy. Withania somnifera (WS) extract has been reported to have potent antioxidant and free radical quenching properties in various disease conditions. The present study evaluated the hypothesis that WS extract would reduce oxidative stress-associated neurodegeneration after intracerebroventricular injection of streptozotocin (ICV-STZ) in rats. To test this hypothesis, male Wistar rats were pretreated with WS extract at doses of 100, 200, and 300 mg/kg body weight once daily for 3 weeks. On day 22nd, the rats were infused bilaterally with ICV-STZ injection (3 mg/kg body weight) in normal saline while sham group received only saline. Two weeks after the lesioning, STZ-infused rats showed cognitive impairment in the Morris water maze test. The rats were sacrificed after 3 weeks of the lesioning for the estimation of the contents of lipid peroxidation, reduced glutathione, and activities of glutathione reductase, glutathione peroxidase, and catalase. Pretreatment with WS extract attenuated behavioral, biochemical, and histological alterations significantly in dose-dependent manner in the hippocampus and cerebral cortex of ICV-STZ-infused rats. These results suggest that WS affords a beneficial effect on cognitive deficit by ameliorating oxidative damage induced by streptozotocin in a model of cognitive impairment.
机译:氧化应激是与年龄相关的神经退行性疾病的关键因素。因此,抑制造成慢性有害神经变性的氧化损伤是神经保护疗法的重要策略。据报道,Withania somnifera(WS)提取物在各种疾病条件下均具有有效的抗氧化剂和自由基猝灭特性。本研究评估了以下假设:WS提取物可减少大鼠脑室内注射链脲佐菌素(ICV-STZ)后氧化应激相关的神经变性。为了验证这一假设,雄性Wistar大鼠用WS提取物预处理,剂量为100、200和300 mg / kg体重,每天一次,持续3周。在第22天,向大鼠双侧注射生理盐水中的ICV-STZ注射液(3mg / kg体重),而假手术组仅接受盐水。损伤后两周,注入STZ的大鼠在莫里斯水迷宫测试中显示出认知障碍。损伤3周后处死大鼠,以估计脂质过氧化的含量,还原的谷胱甘肽和谷胱甘肽还原酶,谷胱甘肽过氧化物酶和过氧化氢酶的活性。 WS提取物预处理对ICV-STZ注入大鼠海马和大脑皮层的行为,生化和组织学改变具有明显的剂量依赖性。这些结果表明,WS通过改善在认知障碍模型中链脲佐菌素引起的氧化损伤,对认知缺陷提供有益的作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号