Neurocognitive Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Neurocognitive Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Life Sci. 2016 Dec 15;167:46-56. doi: 10.1016/j.lfs.2016.10.026. Epub 2016 Oct 26.
Renin-angiotensin system has a role in inflammation and also involves in learning and memory. In the present study, the effects of captopril on lipopolysaccharide (LPS) induced learning and memory impairments, hippocampal cytokine levels and brain tissues oxidative damage was investigated.
The rats were divided and treated : [1] saline (Control), [2] LPS (1mg/kg), [3-5] 10, 50 or 100mg/kg captopril 30min before LPS. The treatment was started since six days before the behavioral experiments and continued during the behavioral tests (LPS injection two h before each behavioral experiment).
Administration of LPS prolonged the escape latency and traveled path to find the platform in Morris water maze (MWM) test (P<0.01-P<0.001) while, shortened the latency to enter the dark compartment in passive avoidance (PA) test (P<0.001). Pretreatment by all doses of captopril improved performances of the rats in MWM (P<0.05-P<0.001) and also prolonged the latency to enter the dark in PA test (P<0.001). LPS also increased IL-6, TNF-α, malondialdehyde (MDA) and nitric oxide(NO) metabolites in the hippocampal tissues (P<0.05-P<0.001) which were prevented by captopril (P<0.05-P<0.001). The thiol, superoxide dismutase(SOD) and catalase(CAT) in the hippocampus of LPS group were lower than the control (P<0.001) while, they were enhanced when the aniamls were pretraeted by captopril (P<0.01-P<0.001).
The results of present study showed that captopril improved the LPS-induced learning and memory impairments in rats which were accompanied with attenuating hippocampal cytokine levels and improving the brain tissues oxidative damage criteria.
肾素-血管紧张素系统在炎症中起作用，也参与学习和记忆。在本研究中，研究了卡托普利对脂多糖（LPS）诱导的学习和记忆障碍、海马细胞因子水平和脑组织氧化损伤的影响。
将大鼠分为以下几组并进行处理：[1]生理盐水（对照），[2]LPS（1mg/kg），[3-5]10、50 或 100mg/kg 卡托普利，在 LPS 前 30 分钟给药。治疗从行为实验前六天开始，并在行为实验期间继续（LPS 注射在每次行为实验前两小时）。
LPS 给药延长了 Morris 水迷宫（MWM）测试中的逃避潜伏期和寻找平台的路径（P<0.01-P<0.001），同时缩短了被动回避（PA）测试中进入黑暗隔间的潜伏期（P<0.001）。所有剂量的卡托普利预处理均改善了大鼠在 MWM 中的表现（P<0.05-P<0.001），并延长了 PA 测试中进入黑暗的潜伏期（P<0.001）。LPS 还增加了海马组织中的白细胞介素 6、肿瘤坏死因子-α、丙二醛（MDA）和一氧化氮（NO）代谢物（P<0.05-P<0.001），这些物质被卡托普利阻止（P<0.05-P<0.001）。LPS 组的海马组织中的硫醇、超氧化物歧化酶（SOD）和过氧化氢酶（CAT）低于对照组（P<0.001），而当动物用卡托普利预处理时，这些物质则增强（P<0.01-P<0.001）。
本研究结果表明，卡托普利改善了 LPS 诱导的大鼠学习和记忆障碍，同时减轻了海马细胞因子水平，并改善了脑组织氧化损伤指标。
