Pelargonidin improves memory deficit in amyloid β25-35 rat model of Alzheimer’s disease by inhibition of glial activation, cholinesterase, and oxidative stress

详细信息    查看全文

• 作者：Hamid Sohanaki^a ; Tourandokht Baluchnejadmojarad^b ; ^{tmojarad@yahoo.com" class="auth_mail" title="E-mail the corresponding author} ; Farnaz Nikbakht^b ; Mehrdad Roghani^c ; ^{mehjour@shahed.ac.ir" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Pelargonidin ; β amyloid ; Oxidative stress ; Glial fibrillary acidic protein ; Acetylcholinesterase ; Inducible nitric oxide synthase
• 刊名：Biomedicine & Pharmacotherapy
• 出版年：2016
• 出版时间：October 2016
• 年：2016
• 卷：83
• 期：Complete
• 页码：85-91
• 全文大小：844 K

文摘

Alzheimer’s disease (AD) is a multifactorial disorder with devastating outcomes and few mostly palliative available therapeutic strategies. Pelargonidin (Pel), an anthocyanin compound, is an estrogen receptor agonist with lower side effects versus estrogen. This study examined neuroprotective effect of Pel on intrahippocampal amyloid β25-35 (Aβ) rat model of AD. Rats were divided into groups of sham, Aβ, and Pel-pretreated Aβ (10 mg/kg; p.o.). Animals underwent Morris water maze (MWM) test in addition to measurement of hippocampal oxidative stress, acetylcholinesterase (AChE) activity, glial fibrillary acidic protein (GFAP) and inducible nitric oxide synthase (iNOS). Pel pretreatment of Aβ group significantly improved escape latency and distance swum in MWM versus Aβ group and attenuated hippocampal malondialdehyde (MDA) and increased catalase activity with no significant change of nitrite. Meanwhile, Pel improved hippocampal AChE activity and lowered GFAP level with no significant change of iNOS. Our results suggest that Pel could improve Aβ25-35-induced memory deficit through mitigation of oxidative stress, cholinergic dysfunction, and astrocyte reaction.