A glucan isolated from flowers of Lonicera japonica Thunb. inhibits aggregation and neurotoxicity of Aβ42

Wang, Peipei; Liao, Weiqi; Fang, Jianping; Liu, Qin; Yao, Jian; Hu, Minghua; Ding, Kan

doi:10.1016/j.carbpol.2014.03.060

Cited by 86 publications

(48 citation statements)

References 34 publications

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“…Apomorphine [299] , melatonin [300] , and tannic acid [301] can prevent Aβ aggregation. A number of small mol- [302] . Resveratrol, curcumin, EGb761, isoliquiritigenin, protocatechuic acid, atractylenolide III, chlorogenic acid, euphorbiafactor L3, euphorbiafactor L2, ganoderic acid D, and ganoderic acid DM extracts from Chinese herbal medicine can inhibit Aβ aggregation [303,304] .…”

Section: Anti-aggregation Agentsmentioning

confidence: 99%

Amyloid beta: structure, biology and structure-based therapeutic development

et al. 2017

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Amyloid beta peptide (Aβ) is produced through the proteolytic processing of a transmembrane protein, amyloid precursor protein (APP), by β-and γ-secretases. Aβ accumulation in the brain is proposed to be an early toxic event in the pathogenesis of Alzheimer's disease, which is the most common form of dementia associated with plaques and tangles in the brain. Currently, it is unclear what the physiological and pathological forms of Aβ are and by what mechanism Aβ causes dementia. Moreover, there are no efficient drugs to stop or reverse the progression of Alzheimer's disease. In this paper, we review the structures, biological functions, and neurotoxicity role of Aβ. We also discuss the potential receptors that interact with Aβ and mediate Aβ intake, clearance, and metabolism. Additionally, we summarize the therapeutic developments and recent advances of different strategies for treating Alzheimer's disease. Finally, we will report on the progress in searching for novel, potentially effective agents as well as selected promising strategies for the treatment of Alzheimer's disease. These prospects include agents acting on Aβ, its receptors and tau protein, such as small molecules, vaccines and antibodies against Aβ; inhibitors or modulators of β-and γ-secretase; Aβ-degrading proteases; tau protein inhibitors and vaccines; amyloid dyes and microRNAs.

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Section: Anti-aggregation Agentsmentioning

confidence: 99%

Amyloid beta: structure, biology and structure-based therapeutic development

et al. 2017

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“…Recently, ethanolic extracts of LJ were shown to inhibit aggregation and neurotoxicity of amyloid beta (Ab ) in human neuroblastoma cells. 18 In addition, it was previously reported that methanolic extracts of LJ have neuroprotective activity against glutamate-induced neurotoxicity in primary cultured rat cortical cells. 19 In our previous studies, we also demonstrated the effect of LJ in promoting oxidative stress-induced neuronal cell death through activation of MAPKs, PI3K/Akt, and NF-jB in SH-SY5Y cellular models.…”

Section: Introduction Mmentioning

confidence: 99%

Lonicera japonicaTHUNB. Extract Inhibits Lipopolysaccharide-Stimulated Inflammatory Responses by Suppressing NF-κB Signaling in BV-2 Microglial Cells

Kwon

Hong

et al. 2015

Journal of Medicinal Food

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In the current study, we evaluated the anti-inflammatory effects of Lonicera japonica THUNB. (LJ) and its underlying molecular mechanism in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. Our results indicated that LJ significantly inhibits LPS-stimulated production of nitric oxide (NO) and prostaglandin E2 (PGE2). In addition, LJ inhibited inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at both the protein and mRNA levels. In LPSstimulated BV-2 microglial cells, LJ inhibited proinflammatory cytokines and chemokines, tumor necrosis factor-a (TNF-a), interleukin-1b (IL-1b), monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinase-9 (MMP-9) enzymatic activities, and/or mRNA expression, as well as reactive oxygen species (ROS) production. LJ significantly suppressed activation of nuclear factor-jB (NF-jB) and its translocation from the cytosol to the nucleus and suppressed the DNA-binding activity of NF-jB. Furthermore, LJ significantly inhibited phosphorylation of c-Jun N-terminal kinase ( JNK), extracellular signalregulated kinase 1/2 (ERK 1/2), p38 mitogen-activated protein kinases (MAPKs), phosphatidylinositol 3-kinases (PI3K)/Akt, and Janus kinase 1 ( JAK1)/signal transducer and activator of transcription (STAT)1/3. Collectively, our findings indicated that the antineuroinflammatory properties of LJ in LPS-induced BV-2 microglial cells is due to downregulation of proinflammatory cytokines and chemokines downstream of inhibition of NF-jB activation.

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“…Samples (35 mg) were dissolved and deutero-exchanged with D 2 O, and then redissolved in 0.5 ml D 2 O. The 1 H, 13 C NMR spectra and two-dimensional spectra (HSQC, HMBC, 1 H-1 H COSY) were measured at 25 • C with acetone as internal standard (31.5 ppm for carbon, 2.26 ppm for hydrogen).…”

Section: Nmr and Esi-msmentioning

confidence: 99%

“…After cooled to room temperature, the solution was neutralized with 0.3 M HCl (200 l) and distilled water was added to make the total volume to 2 ml, which was washed with CHCl 3 (2 ml) for three times. The water phase was then filtered by 0.22 m filter membrane and analyzed by HPLC [13]. The monosaccharide standards were processed and analyzed in parallel as samples.…”

Section: Monosaccharide Composition Analysismentioning

confidence: 99%