Research Paper Volume 10, Issue 11 pp 3229—3248
Methanolic extract of Tamarix Gallica attenuates hyperhomocysteinemia induced AD-like pathology and cognitive impairments in rats
- 1 Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
- 2 Cognitive Impairment Ward of Neurology Department, The Third Affiliated Hospital of Shenzhen University, Shenzhen, 518001, Guangdong Province, China
- 3 Co-innovation Center of Neuroregeneration, Nantong University, Nantong, JS, 226001, China
- 4 Department of Genetics and Genomic Sciences, Icahn Institute of Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
received: August 22, 2018 ; accepted: October 27, 2018 ; published: November 12, 2018 ;https://doi.org/10.18632/aging.101627
How to Cite
Copyright: Salissou et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Although few drugs are available today for the management of Alzheimer’s disease (AD) and many plants and their extracts are extensively employed in animals’ studies and AD patients, yet no drug or plant extract is able to reverse AD symptoms adequately. In the present study, Tamarix gallica (TG), a naturally occurring plant known for its strong antioxidative, anti-inflammatory and anti-amyloidogenic properties, was evaluated on homocysteine (Hcy) induced AD-like pathology and cognitive impairments in rats. We found that TG attenuated Hcy-induced oxidative stress and memory deficits. TG also improved neurodegeneration and neuroinflammation by upregulating synaptic proteins such as PSD95 and synapsin 1 and downregulating inflammatory markers including CD68 and GFAP with concomitant decrease in proinflammatory mediators interlukin-1β (IL1β) and tumor necrosis factor α (TNFα). TG attenuated tau hyperphosphorylation at multiple AD-related sites through decreasing some kinases and increasing phosphatase activities. Moreover, TG rescued amyloid-β (Aβ) pathology through downregulating BACE1. Our data for the first time provide evidence that TG attenuates Hcy-induced AD-like pathological changes and cognitive impairments, making TG a promising candidate for the treatment of AD-associated pathological changes.
3×Tg mice: Triple transgenic mice; AD: Alzheimer’s disease; APP: Amyloid precursor protein; Aβ: Amyloid-β; BACE1: Beta amyloid precursor protein cleaving enzyme 1; BCA: Bicinchoninic acid; CaMKII: Ca2+/calmodulin-dependent protein kinase II; CaMKII-pT286: Phosphorylated-CaMKII at threonine 286; CD68: Cluster of Differentiation 68; CDK5: Cyclin dependent kinase 5; CXA: chloroform, xylene, alcohol; ELISA: Enzyme-linked immunosorbent assay; GFAP: Glial fibrillary acidic protein; GSK3β: Glycogen synthase kinase-3β; Hcy: Homocysteine; HHcy: Hyperhomocysteinemia; HRP: Avidin-Horseradish Peroxidase; IL1β: Interleukin1 Beta; KGlcA: kaempferol 3-O-β-D-glucuronide; KGlcA-Me: kaempferol 3-O-β-D-glucuronide methyl ester; MDA: Malondialdehyde; MWM: Morris Water Maze; NFTs: Neurofibrillary tangles; NMDA: N-methyl-D-aspartate; PP2A: Protein phosphatase 2A; PP2Ac: Protein phosphatase 2A c subunit; PSD: Postsynaptic density; QGlcA: quercetin 3-O-β-D-glucuronide; QGlcA-Me: quercetin 3-O-β-D-glucuronide methyl; ROS: reactive oxygen species; SD: Sprague-Dawley; SOD: Superoxide dismutase; STAT3: Signal transducer and activator of transcription 3; TBA: Thiobarbituric Acid; TG: Tamarix Gallica; TNFα: Tumor Necrosis Factor Alpha.