Emad Shaista, Qadeer Sara, Sadaf Sana, Batool Zehra, Haider Saida, Perveen Tahira
Neurochemistry and Biochemical Neuropharmacology Research Unit, Department of Biochemistry, University of Karachi, Karachi, Sindh, Pakistan.
Neurochemistry and Biochemical Neuropharmacology Research Unit, Department of Biochemistry, University of Karachi, Karachi, Sindh, Pakistan.
Pharmacol Rep. 2017 Apr;69(2):300-305. doi: 10.1016/j.pharep.2016.11.009. Epub 2016 Nov 29.
Repeated stress paradigms have been shown to cause devastating alterations on memory functions. Stress is linked with inflammation. Psychological and certain physical stressors could lead to neuroinflammation. Inflammatory process may occur by release of mediators and stimulate the production of prostaglandins through cyclooxygenase (COX). Treatment with COX inhibitors, which restrain prostaglandin production, has enhanced memory in a number of neuroinflammatory states showing a potential function for raised prostaglandins in these memory shortfalls. In the present study, potential therapeutic effects of indomethacin and diclofenac sodium on memory in both unrestraint and restraint rats were observed.
Two components, long term memory and short term memory were examined by Morris water maze (MWM) and elevated plus maze (EPM) respectively. The present study also demonstrated the effect of nonsteroidal anti-inflammatory drugs (NSAIDs) on lipid peroxidation (LPO) and activities of antioxidant enzymes along with the activity of acetylcholinesterase (AChE). Results of MWM and EPM showed significant effects of drugs in both unrestraint and restraint rats as escape latency and transfer latency, in respective behavioral models were decreased as compared to that of control. This study also showed NSAIDs administration decreased LPO and increased antioxidant enzymes activity and decreased AChE activity in rats exposed to repeated stress.
In conclusion this study suggests a therapeutic potential of indomethacin and diclofenac against repeated stress-induced memory deficits.
反复应激范式已被证明会对记忆功能造成破坏性改变。应激与炎症相关。心理和某些身体应激源可导致神经炎症。炎症过程可能通过介质释放而发生，并通过环氧化酶（COX）刺激前列腺素的产生。用抑制前列腺素产生的COX抑制剂进行治疗，已在多种神经炎症状态下增强了记忆，这表明升高的前列腺素在这些记忆缺陷中具有潜在作用。在本研究中，观察了吲哚美辛和双氯芬酸钠对无束缚和束缚大鼠记忆的潜在治疗作用。
分别通过莫里斯水迷宫（MWM）和高架十字迷宫（EPM）检测长期记忆和短期记忆这两个方面。本研究还证明了非甾体抗炎药（NSAIDs）对脂质过氧化（LPO）、抗氧化酶活性以及乙酰胆碱酯酶（AChE）活性的影响。MWM和EPM的结果显示，药物对无束缚和束缚大鼠均有显著影响，在各自的行为模型中，与对照组相比，逃避潜伏期和转移潜伏期均缩短。本研究还表明，给予NSAIDs可降低反复应激大鼠的LPO水平，增加抗氧化酶活性，并降低AChE活性。
总之，本研究表明吲哚美辛和双氯芬酸对反复应激诱导的记忆缺陷具有治疗潜力。
