Tenuifolin, an extract derived from <i>tenuigenin</i>, inhibits amyloid‐β secretion <i>in vitro</i>

Lv, Jiajia; Jia, Honglin; Jiang, Yong; Ruan, Yan; Liu, Z.; Yue, Wencong; Beyreuther, Konrad; Tu, Peng‐Fei; Zhang, D.

doi:10.1111/j.1748-1716.2009.01961.x

Cited by 68 publications

(46 citation statements)

References 24 publications

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“…Tenuigenin is the active component from the roots of Polygala tenuifolia Willd and shares many of its effects, such as the facilitation of memory and treatment of agerelated declines in function [22].…”

Section: Discussionmentioning

confidence: 99%

Tenuigenin Promotes Proliferation and Differentiation of Hippocampal Neural Stem Cells

et al. 2011

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The present study was to investigate the influence of tenuigenin, an active ingredient of Polygala tenuifolia Willd, on the proliferation and differentiation of hippocampal neural stem cells in vitro. Tenuigenin was added to a neurosphere culture and neurosphere growth was measured using MTT assay. The influence of tenuigenin on the proliferation of neural progenitors was examined by Clone forming assay and BrdU detection. In addition, the differentiation of neural stem cells was compared using immunocytochemistry for β III-tubulin and GFAP. The results showed that addition of tenuigenin to the neural stem cell medium increased the number of newly formed neurospheres. More neurons were also obtained when tenuigenin was added in the differentiation medium. These findings suggest that tenuigenin is involved in regulating the proliferation and differentiation of hippocampal neural stem cells. This result may be one of the underlying reasons for tenuigenin's nootropic and anti-aging effects.

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Section: Discussionmentioning

confidence: 99%

Tenuigenin Promotes Proliferation and Differentiation of Hippocampal Neural Stem Cells

et al. 2011

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“…(Polygalaceae) is commonly used as a traditional Chinese medicine to treat memory loss (Lv et al, 2009). An extract of P. tenuifolia was reported to alleviate scopolamine-induced cognitive impairment in rats (Park et al, 2002).…”

Section: β-Secretase Inhibitorsmentioning

confidence: 99%

Potential therapeutic agents against Alzheimer’s disease from natural sources

Park

2010

Arch. Pharm. Res.

106

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The average human life span in developed countries has increased to more than 80 years following rapid breakthrough and developments in modern medicine and science, resulting in prolonged life expectancy and increase in the population counts of the geriatric age group. This translates into a dramatic increase in disease burden of elderly patients suffering from senile disorders including neurodegenerative diseases, particularly Alzheimer's disease (AD). AD is characterized by the death of nerve cells in the cerebral cortex and is the most common subtype of dementia that affected 25 million people worldwide in 2000 and is expected to increase to 114 million by 2050. Despite the exponential growth in the number of AD patients, only acetylcholinesterase (AChE) inhibitors are being currently used to treat AD. It is well known that AChE inhibitors can alleviate the symptoms of AD but not halt the disease progression. Consequently, therapeutic agents against AD acting at various pathologic levels are needed. In the recent decade, natural products with anti-AD properties have attracted much attention. But very few natural products have been investigated in a scientifically justifiable method for these biological activities. Following a detailed research process, it is certain that natural products have a strong potential to develop biologically active compounds with new chemical structures. Many studies have been carried out to identify the naturally occurring anti-AD agents. This review article describes the molecular targets aiming at developing the anti-AD agents including the inhibition of AChE, inhibition of Aβ production by enhancing α-secretase (non-amyloidogenic pathway) or inhibiting β- and γ-secretases (amyloidogenic pathway), alleviating Aβ-induced neurotoxicity or reducing Aβ-induced neuroinflammation. In addition, this paper summarizes the potential of some of the natural products that might inhibit specific molecular targets and slow the progression of this disease.

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“…Recently, P. tenuifolia was reported to provide sedative and anti-dementia neuroprotective efficacy in several in vitro pharmacological studies, as well as anti-oxidative and anti-neurotoxic effects in cultured neurons [14,21,22]. The present study shows that the neuron protective effects of TEN might result from the inhibition of LPS-induced microglial activation and the release of inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 51%

“…In a rat model of Alzheimer's disease (AD), P. tenuifolia root extracts ameliorate spatial cognition disorders and protect neuronal cells against in vitro toxins [18][19][20], as well as improving the cognitive behavior of AD animal models [16]. Cell culture results have shown that treatment with P. tenuifolia decreases secretion of amyloid b-protein, which is responsible for neuronal pathogenesis and cell death in AD [21,22]. BT-11, the extract from P. tenuifolia Willdenow roots, has been shown to ameliorate memory impairment induced by scopolamine and stress in rats [15].…”

Section: Introductionmentioning

confidence: 98%

Tenuigenin Protects Dopaminergic Neurons from Inflammation‐Mediated Damage Induced by the Lipopolysaccharide

Yuan

et al. 2012

CNS Neuroscience & Therapeutics

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Tenuifolin, an extract derived from tenuigenin, inhibits amyloid‐β secretion in vitro

Abstract: Tenuifolin is an effective compound from tenuigenin. We believe that this finding should lead the way for future experiments to determine the exact mechanism for tenuifolin's effect on Abeta secretion.

Cited by 68 publications

References 24 publications

Tenuigenin Promotes Proliferation and Differentiation of Hippocampal Neural Stem Cells

Tenuigenin Promotes Proliferation and Differentiation of Hippocampal Neural Stem Cells

Potential therapeutic agents against Alzheimer’s disease from natural sources

Tenuigenin Protects Dopaminergic Neurons from Inflammation‐Mediated Damage Induced by the Lipopolysaccharide

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