Protective effects of Ginkgo biloba extract (EGb761) and its constituents quercetin and ginkgolide B against β-amyloid peptide-induced toxicity in SH-SY5Y cells

Shi, Chun; Zhao, Lei; Zhu, Bilian; Li, Qianxi; Yew, David T.; Ye, Zhibin; Xu, Jie

doi:10.1016/j.cbi.2009.05.010

Cited by 126 publications

(96 citation statements)

References 52 publications

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“…a P \ 0.01 versus control group (vehicle-only); b P \ 0.01 versus the corresponding insulted group (bilobalide-and LY294002-free). (Color figure online) c The ability of bilobalide to modulate phosphorylation of Akt and ERK1/2 As Akt and ERK1/2 are two protein kinases involved in the survival of several cell types [10][11][12][13][14][15][16][17][18], the ability of bilobalide to modulate these two signaling proteins was also investigated. It was found that, 24 h bilobalide treatment dose-dependently increased levels of p-Akt (Ser473 and Thr308) in SH-SY5Y cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Bilobalide could also restore impaired phosphorylation of CREB in Ab-expressing neuroblastoma cells, but the upstream signaling pathways activated by bilobalide still remained unknown [9]. It is known that, protein kinase pathways involved in the survival of several cell types include PKC, ERK and PI3K/Akt pathways [10][11][12][13][14][15][16][17][18], which are also known to be the upstream pathways for CREB activation [9,19]. This suggests to us that the protective effects of bilobalide may be associated with modulation of these pro-survival signaling kinases.…”

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confidence: 98%

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Bilobalide prevents apoptosis through activation of the PI3K/Akt pathway in SH-SY5Y cells

Shi

Yew

et al. 2010

Apoptosis

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Bilobalide, a sesquiterpene trilactone constituent of Ginkgo biloba leaf extracts, has been proposed to exert protective and trophic effects on neurons. However, mechanisms underlying the protective effects of bilobalide remain unclear. Using human SH-SY5Y neuroblastoma cells and primary hippocampal neurons, this study investigated the neuroprotective effects of bilobalide. We mimicked aging-associated neuronal impairments by applying external factors (beta amyloid protein (Abeta) 1-42, H(2)O(2) and serum deprivation) consequently inducing cell apoptosis. As markers for apoptosis, cell viability, DNA fragmentation, mitochondrial membrane potential and levels of cleaved caspase 3 were measured. We found that, bilobalide prevented Abeta 1-42-, H(2)O(2)- and serum deprivation-induced apoptosis. To better understand the neuroprotective effects of bilobalide, we also tested the ability of bilobalide to modulate pro-survival signaling pathways such as protein kinase C (PKC), extracellular-regulated kinase 1/2 (ERK1/2) and phosphatidylinositol 3-kinase (PI3K)/Akt pathways. It was found that, bilobalide dose-dependently increased PI3K activity and levels of phosphorylated Akt (p-Akt Ser473 and Thr308), which could be maintained up to at least 2 h after bilobalide withdrawal in cells treated with or without Abeta 1-42, H(2)O(2) or serum-free medium. In addition, application of PI3K/Akt inhibitor LY294002 could abrogate both the protective effects of bilobalide against Abeta 1-42-, H(2)O(2)- and serum deprivation-induced apoptotic cell damage and bilobalide-induced increase in PI3K activity and levels of p-Akt (Ser473 and Thr308). In contrast, application of PKC inhibitor staurosporine (STS) did not affect the protective effects of bilobalide. Moreover, no change in levels of phosphorylated ERK1/2 (p-ERK1/2) was observed in bilobalide-treated cells. These results further suggested that the PI3K/Akt pathway might be involved in the protective effects of bilobalide. Since modern technology allows production of purified bilobalide with high bioavailability, bilobalide may be useful in developing therapy for diseases involving age-associated neurodegeneration.

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 98%

Bilobalide prevents apoptosis through activation of the PI3K/Akt pathway in SH-SY5Y cells

Shi

Yew

et al. 2010

Apoptosis

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“…Additionally, mitochondrial dysfunction is suggested to be involved in Ab-induced oxidative cell death (Atamna and Frey 2007;Cardoso et al 2001;Ferrer 2009;Yang et al 2008). Furthermore, various types of compounds, such as acteoside, ginkgolide, and galantamine, have been shown to inhibit Ab-induced neurotoxicity (Liu et al 2009;Matharu et al 2009;Shi et al 2009;Wang et al 2009). …”

Section: Introductionmentioning

confidence: 95%

3,4,5-tri-O-caffeoylquinic acid inhibits amyloid β-mediated cellular toxicity on SH-SY5Y cells through the upregulation of PGAM1 and G3PDH

et al. 2011

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Caffeoylquinic acid (CQA) is one of the phenylpropanoids found in a variety of natural resources and foods, such as sweet potatoes, propolis, and coffee. Previously, we reported that 3,5-di-O-caffeoylquinic acid (3,5-di-CQA) has a neuroprotective effect against amyloid-β (Aβ)-induced cell death through the overexpression of glycolytic enzyme. Additionally, 3,5-di-CQA administration induced the improvement of spatial learning and memory on senescence accelerated-prone mice (SAMP8). The aim of this study was to investigate whether 3,4,5-tri-O-caffeoylquinic acid (3,4,5-tri-CQA), isolated from propolis, shows a neuroprotective effect against Aβ-induced cell death on human neuroblastoma SH-SY5Y cells. To clarify the possible mechanism, we performed proteomics and real-time RT-PCR as well as a measurement of the intracellular adenosine triphosphate (ATP) level. These results showed that 3,4,5-tri-CQA attenuated the cytotoxicity and prevented Aβ-mediated apoptosis. Glycolytic enzymes, phosphoglycerate mutase 1 (PGAM1) and glyceraldehyde-3-phosphate dehydrogenase (G3PDH) were overexpressed in co-treated cells with both 3,4,5-tri-CQA and Aβ. The mRNA expression of PGAM1, G3PDH, and phosphoglycerate kinase 1 (PGK1), and intracellular ATP level were also increased in 3,4,5-tri-CQA treated cells. Taken together the findings in our study suggests that 3,4,5-tri-CQA shows a neuroprotective effect against Aβ-induced cell death through the upregulation of glycolytic enzyme mRNA as well as ATP production activation.

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“…In addition, pinostrobin has strong antioxidant effect in vitro (Fahey and Stephenson 2002). Several antioxidants and free radical scavengers, including Folium Ginkgo Biloba (Shi et al 2009), huperzine A (Gao and Tang 2006), and curcumin (Park et al 2008), have been reported to attenuate the toxicity induced by Ab. It is therefore hypothesized that pinostrobin may also possess protective action against Ab toxicity.…”

Section: Introductionmentioning

confidence: 97%

Protective Effects of Pinostrobin on β-Amyloid-Induced Neurotoxicity in PC12 Cells

Xian

Lin

et al. 2012

Cell Mol Neurobiol

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Beta-Amyloid peptide (Aβ), a major protein component of brain senile plaques in Alzheimer's disease (AD), has been considered as a critical cause in the pathogenesis of AD. Pinostrobin, a potent flavonoid inducer, is the major and most active ingredient of Folium cajani. The present study aimed to investigate whether pinostrobin could provide protective effect against Aβ(25-35)-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. The PC12 cells were pretreated with different concentrations of pinostrobin for 2 h, followed by the challenge with 20 μM Aβ(25-35) for 24 h. The results showed that pretreatment with pinostrobin significantly elevated cell viability, decreased the lactate dehydrogenase activity, the levels of intracellular reactive oxygen species and calcium, and mitochondrial membrane potential in Aβ(25-35)-treated PC12 cells. In addition, pinostrobin significantly suppressed the formation of DNA fragmentation and increased the ratio of Bcl-2/Bax. These results indicate that pinostrobin was able to exert a neuroprotective effect against Aβ(25-35)-induced neurotoxicity in PC12 cells, at least in part, via inhibiting oxidative damage and calcium overload, as well as suppressing the mitochondrial pathway of cellular apoptosis.

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Protective effects of Ginkgo biloba extract (EGb761) and its constituents quercetin and ginkgolide B against β-amyloid peptide-induced toxicity in SH-SY5Y cells

Cited by 126 publications

References 52 publications

Bilobalide prevents apoptosis through activation of the PI3K/Akt pathway in SH-SY5Y cells

Bilobalide prevents apoptosis through activation of the PI3K/Akt pathway in SH-SY5Y cells

3,4,5-tri-O-caffeoylquinic acid inhibits amyloid β-mediated cellular toxicity on SH-SY5Y cells through the upregulation of PGAM1 and G3PDH

Protective Effects of Pinostrobin on β-Amyloid-Induced Neurotoxicity in PC12 Cells

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