Cassia obtusifolia seed ameliorates amyloid β-induced synaptic dysfunction through anti-inflammatory and Akt/GSK-3β pathways

被引:40
作者
Yi, Jee Hyun [1 ]
Park, Hey Jin [2 ,3 ]
Lee, Seungheon [4 ]
Jung, Ji Wook [5 ]
Kim, Byeong C. [6 ]
Lee, Young Choon [2 ,3 ]
Ryu, Jong Hoon [7 ,8 ]
Kim, Dong Hyun [2 ,3 ]
机构
[1] Univ Bristol, Fac Med & Dent, Sch Clin Sci, Bristol, Avon, England
[2] Dong A Univ, Dept Med Biotechnol, Coll Hlth Sci, Busan 604714, South Korea
[3] Dong A Univ, Inst Convergence Biohlth, Busan 604714, South Korea
[4] Jeju Natl Univ, Sch Marine Biomed Sci, Dept Aquat Biomed Sci, Coll Ocean Sci, Jeju 690756, South Korea
[5] Daegu Haany Univ, Dept Herbal Med Pharmacol, Coll Herbal Bioind, Kyungsan 712715, South Korea
[6] Chonnam Natl Univ Hosp, Biomed Res Inst, Chonnam Bristol Frontier Lab, Jebong Ro 501757, Gwangju, South Korea
[7] Kyung Hee Univ, Dept Life & Nanopharmaceut Sci, Coll Pharm, Seoul 130701, South Korea
[8] Kyung Hee Univ, Dept Oriental Pharmaceut Sci, Coll Pharm, Seoul 130701, South Korea
关键词
Cassia obtusifolia seeds; Amyloid beta; Long-term potentiation; Recognition memory; LONG-TERM POTENTIATION; ALZHEIMERS-DISEASE; A-BETA; MEDIATED SUPPRESSION; MEDICINAL-PLANTS; OXIDATIVE STRESS; TORA L; PLASTICITY; PROTEIN; MEMORY;
D O I
10.1016/j.jep.2015.12.007
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Ethnopharmacological relevance: Tea infused with the seed of Cassia obtusifolia has been traditionally used as an herbal remedy for liver, eye, and acute inflammatory diseases. Recent pharmacological reports have indicated that Cassiae semen has neuroprotective effects, attributable to its anti-inflammatory actions, in ischemic stroke and Parkinson's disease models. Aim of the study: Previously, the ethanol extract of C. obtusifolia seeds (COE) was reported to have memory enhancing properties. However, the effects of COE in an Alzheimer's disease (AD) model are currently unknown. In this study, we investigated the effect(s) of COE on aberrant synaptic plasticity and memory impairment induced by amyloid beta (A beta), a key toxic component found in the AD brain. Materials and methods: To determine the effect of COE on A beta-induced aberrant synaptic plasticity, we used acute mouse hippocampal slices and delivered theta burst stimulation to induce long-term potentiation (LTP). Western blots were used to detect A beta- and/or COE-induced changes in signaling proteins. The novel object location recognition test was conducted to determine the effect of COE on A(3 induced recognition memory impairment. Results: COE was found to ameliorate A beta-induced LTP impairment in the acute hippocampal slices. Glycogen synthase kinase-3 beta (GSK-3 beta), a key molecule in LTP impairment, was activated by A beta. However, this process was inhibited by COE via Akt signaling. Moreover, COE was found to attenuate A beta-induced microglia, inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX) activation. In the in vivo studies performed, COE ameliorated the A beta-induced object recognition memory impairment. Conclusion: These results suggest that COE, exhibits neuroprotective activities against A beta-induced brain disorders. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:50 / 57
页数:8
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