Protocatechuic acid improves cognitive deficits and attenuates amyloid deposits, inflammatory response in aged AβPP/PS1 double transgenic mice

被引:59
作者
Song, Yu [1 ]
Cui, Taizhen [1 ]
Xie, Na [2 ]
Zhang, Xiaoyi [1 ]
Qian, Zhibin [2 ]
Liu, Juyuan [1 ]
机构
[1] Xinxiang Med Univ, Sch Pharm, Xinxiang 453003, Henan Province, Peoples R China
[2] Xinxiang Med Univ, Affiliated Hosp 3, Dept Cardiol, Xinxiang 453003, Henan Province, Peoples R China
关键词
Protocatechuic acid; Alzheimer's disease; Cognitive deficits; Inflammation; Amyloid-beta; ALZHEIMERS-DISEASE; MITOCHONDRIAL DYSFUNCTION; NEUROTROPHIC FACTOR; OXIDATIVE STRESS; MOUSE MODEL; IN-VITRO; BRAIN; AMYLOIDOGENESIS; DEMENTIA; PREVENTS;
D O I
10.1016/j.intimp.2014.03.006
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Protocatechuic acid (PCA), a phenolic compound of Radix Salviae Miltiorrhizae (RSM), has been found to have a protective effect on improving cognitive deficits in STZ-induced AD rats. The present study aimed to evaluate the potential protection activity of PCA on improving cognitive deficits and attenuating A beta deposition and inflammatory responses in aged A beta PP/PS1 double transgenic AD-model mice. The results of Morris water maze test showed that PCA (100 mg/kg) significantly prolonged the mean latency time and the path length of A beta PP/PS1 mice. PCA could significantly reduce the number of A beta positive expressions in the hippocampus and cerebral cortex of A beta PP/PS1 mice by immunocytochemical assay with Congo red staining and decrease remarkably APP expression level by Western blot analysis (P < 0.01). The results from ELISA and Western blot analysis showed that the levels of inflammatory cytokines including TNF-alpha, IL-1 beta, IL-6 and IL-8 decreased remarkably by the treatment with PCA (P < 0.01). Further, there was a substantial increase of brain derived neurotrophic factor (BDNF) in the hippocampus and cerebral cortex of A beta PP/PS1 mice treated with PCA (P < 0.01). The present study provided confirmatory evidence that PCA significantly decreased A beta deposits, APP and inflammatory response, whereas increased learning and memory ability, as well as enhanced BDNF level. Our findings indicated that PCA is an effective neuroprotective agent for AD therapy. It might be associated with the attenuation on A beta deposits and inflammation responses involved in the process. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:276 / 281
页数:6
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