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Effect of phosphamidon on cognition and oxidative stress and its modulation by ascorbic acid and 4??-chlorodiazepam in rats

机译:磷氨酮对抗坏血酸和4μs - 氯二噻嗪对认知和氧化应激及其调节的影响

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Neurosteroids and micronutrient are known to possess neuromodulator and neuroprotective activities. The present study was designed to investigate the effect of 4??-chlorodiazepam (4CD) or ascorbic acid (Vit C) on phosphamidon (PM) induced modulation of cognitive function and oxidative stress in male Wistar rats. Cognitive function was measured by using step-down latency (SDL) on a continuous avoidance apparatus and transfer latency (TL) on an elevated plus maze. Oxidative stress was estimated by measuring brain malondialdehyde (MDA) level, protein carbonyl (PC) and reduced glutathione (GSH) activity. A significant reduction in both acquisition and retention in SDL was found for the PM treated group at weeks 6 and 8 as compared to the control (p < 0.001). PM caused a significant prolongation in both acquisition and retention in TL at 6 and 8 weeks as compared to the control (p < 0.001). Two-week treatment of 4CD or Vit C antagonized the effect of PM on SDL and TL at 8th week. PM produced a statistically significant increase in the brain MDA and PC levels (p < 0.001) and a significant decrease in the brain GSH activity (p < 0.001). Treatment with 4CD or Vit C attenuated the effect of PM on MDA, PC and GSH activities. Results of this study suggest that Vit C and 4CD have potential in reversing cognitive dysfunction and oxidative stress induced by toxicants like PM in the brain. ? 2012 Elsevier Inc. All rights reserved.
机译:已知神经活体和微量营养素具有神经调节剂和神经保护活性。本研究旨在探讨4 ?? - 氯二噻嗪(4CD)或抗坏血酸(VIT C)对磷酸氨基(PM)诱导的阳性Wistar大鼠氧化胁迫调节的影响。通过在连续避免装置上使用降压等待时间(SDL)来测量认知功能,并在升高的加迷宫上传递延迟(TL)。通过测量脑丙二醛(MDA)水平,蛋白质羰基(PC)和降低的谷胱甘肽(GSH)活性来估算氧化应激。与对照相比,在第6周和第8周内发现PM治疗组(P <0.001),发现了在PM治疗组中进行的显着减少了SDL。 PM在与对照相比,在6和8周内在TL中引起显着的延长(P <0.001)。 4CD或VIT C对拮抗PM对SDL和TL的效果的两周治疗在第8周。 PM在脑MDA和PC水平(P <0.001)中产生了统计学显着的增加,并且脑GSH活性的显着降低(P <0.001)。用4CD或VIT C治疗减少PM对MDA,PC和GSH活动的影响。该研究的结果表明Vit C和4CD具有促进毒性诱导的认知功能障碍和毒性诱导的毒性诱导的氧化应激。还2012年elsevier Inc.保留所有权利。

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