Hasanein Parisa, Mahtaj Azam Kazemian
Department of Biology, School of Basic Sciences, Bu-Ali Sina University, Hamedan, Iran.
Department of Biology, School of Basic Sciences, Bu-Ali Sina University, Hamedan, Iran.
Neurosci Lett. 2015 Jan 12;585:23-7. doi: 10.1016/j.neulet.2014.11.027. Epub 2014 Nov 20.
Rosmarinic acid (RA) is a natural phenol that exerts different biological activities, such as antioxidant activity and neuroprotective effects. In this study, we hypothesized that administration of RA (8, 16, and 32 mg/kg, p.o.) for 7 days would effect on scopolamine-induced cognitive dysfunction as an extensively used model of cognitive impairment. The rats were divided into 10 groups. The acquisition trial was done 1h after the last administration of RA. Animals were divided into control, RA (8, 16, and 32 mg/kg) and donepezil (2 mg/kg) treated controls, scopolamine, RA (8, 16, and 32 mg/kg), and donepezil (2 mg/kg) treated scopolamine groups. Memory impairment was induced by scopolamine treatment (1 mg/kg, i.p.) 30 min after the administration of RA, donepezil, or saline. Scopolamine administration caused cognition deficits in the PAL and memory paradigm. While orally RA administration (16 and 32 mg/kg) improved learning and memory in control rats, it reversed learning and memory deficits of scopolamine received groups. Administration of RA at the dose of 8 mg/kg did not alter cognitive function in control and scopolamine treated groups. The combination of anticholinesterase, neuroprotective, and antioxidant properties of RA may all be responsible for the observed effects. These results indicate the beneficial effects of subchronic RA administration in passive avoidance learning and memory in control rats as well as in a pharmacological model of cholinergic deficit which continue to expand the knowledge base in creating new treatment strategies for cognition deficits and dementia. Of course, further studies are warranted for clinical use of RA in the management of demented subjects.
迷迭香酸(RA)是一种天然酚类物质,具有多种生物活性,如抗氧化活性和神经保护作用。在本研究中,我们假设给予RA(8、16和32mg/kg,口服)7天会对东莨菪碱诱导的认知功能障碍产生影响,东莨菪碱诱导的认知功能障碍是一种广泛应用的认知损伤模型。将大鼠分为10组。在最后一次给予RA后1小时进行习得性试验。动物分为对照组、RA(8、16和32mg/kg)和多奈哌齐(2mg/kg)处理的对照组、东莨菪碱组、RA(8、16和32mg/kg)以及多奈哌齐(2mg/kg)处理的东莨菪碱组。在给予RA、多奈哌齐或生理盐水30分钟后,通过腹腔注射东莨菪碱(1mg/kg)诱导记忆损伤。给予东莨菪碱导致在PAL和记忆范式中出现认知缺陷。虽然口服RA(16和32mg/kg)可改善对照大鼠的学习和记忆,但它可逆转接受东莨菪碱组的学习和记忆缺陷。给予8mg/kg剂量的RA并未改变对照组和东莨菪碱处理组的认知功能。RA的抗胆碱酯酶、神经保护和抗氧化特性的综合作用可能是观察到的效果的原因。这些结果表明,亚慢性给予RA对对照大鼠的被动回避学习和记忆以及胆碱能缺陷的药理学模型具有有益作用,这将继续扩大在为认知缺陷和痴呆症制定新治疗策略方面的知识库。当然,RA在痴呆患者管理中的临床应用还需要进一步研究。