Graphene quantum dots for the inhibition of β amyloid aggregation

Liu, Yibiao; Xu, Li-Ping; Dai, Wenhao; Dong, Haifeng; Wen, Yongqiang; Zhang, Xueji

doi:10.1039/c5nr06282a

Cited by 137 publications

(121 citation statements)

References 49 publications

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“…12 These nanomaterials may exert differing degrees of toxicity in animals or cell models depending on the administration route or penetration through physiological barriers such as the BBB. 11,13,14 However, toxicological information on GO materials remains limited. In this study, we examined the neurotoxic effects of graphene family nanomaterials using the PC12 cell model.…”

Section: Discussionmentioning

confidence: 99%

Graphene oxide and reduced graphene oxide induced neural pheochromocytoma-derived PC12 cell lines apoptosis and cell cycle alterations via the ERK signaling pathways

Kang¹,

Liu²,

Wu³

et al. 2017

IJN

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Given the novel applications of graphene materials in biomedical and electronics industry, the health hazards of these particles have attracted extensive worldwide attention. Although many studies have been performed on graphene material-induced toxic effects, toxicological data for the effect of graphene materials on the nervous system are lacking. In this study, we focused on the biological effects of graphene oxide (GO) and reduced graphene oxide (rGO) materials on PC12 cells, a type of traditional neural cell line. We found that GO and rGO exerted significant toxic effects on PC12 cells in a dose- and time-dependent manner. Moreover, apoptosis appeared to be a response to toxicity. A potent increase in the number of PC12 cells at G0/G1 phase after GO and rGO exposure was detected by cell cycle analysis. We found that phosphorylation levels of ERK signaling molecules, which are related to cell cycle regulation and apoptosis, were significantly altered after GO and rGO exposure. In conclusion, our results show that GO has more potent toxic effects than rGO and that apoptosis and cell cycle arrest are the main toxicity responses to GO and rGO treatments, which are likely due to ERK pathway regulation.

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Section: Discussionmentioning

confidence: 99%

Graphene oxide and reduced graphene oxide induced neural pheochromocytoma-derived PC12 cell lines apoptosis and cell cycle alterations via the ERK signaling pathways

Kang¹,

Liu²,

Wu³

et al. 2017

IJN

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“…Matrix-assisted laser desorption/ionization (MALDI) mass spectrometry imaging (MSI) revealed that rGO, with an average diameter of 342 ± 23.5 nm, permeated through the paracellular pathway into the inter-endothelial cleft in a time-dependent manner by decreasing the blood-brain barrier paracellular tightness [63]. In addition, graphene quantum dots (GQDs), with a small size of less than 100 nm, can cross through the blood-brain barrier [64]. Studies on how graphene materials pass through the blood-brain barrier and cause neurotoxicity are very rare, and more data are needed to draw a conclusion.…”

Section: Toxicity Of Gfns (In Vivo and In Vitro)mentioning

confidence: 99%

Toxicity of graphene-family nanoparticles: a general review of the origins and mechanisms

et al. 2016

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Due to their unique physicochemical properties, graphene-family nanomaterials (GFNs) are widely used in many fields, especially in biomedical applications. Currently, many studies have investigated the biocompatibility and toxicity of GFNs in vivo and in intro. Generally, GFNs may exert different degrees of toxicity in animals or cell models by following with different administration routes and penetrating through physiological barriers, subsequently being distributed in tissues or located in cells, eventually being excreted out of the bodies. This review collects studies on the toxic effects of GFNs in several organs and cell models. We also point out that various factors determine the toxicity of GFNs including the lateral size, surface structure, functionalization, charge, impurities, aggregations, and corona effect ect. In addition, several typical mechanisms underlying GFN toxicity have been revealed, for instance, physical destruction, oxidative stress, DNA damage, inflammatory response, apoptosis, autophagy, and necrosis. In these mechanisms, (toll-like receptors-) TLR-, transforming growth factor β- (TGF-β-) and tumor necrosis factor-alpha (TNF-α) dependent-pathways are involved in the signalling pathway network, and oxidative stress plays a crucial role in these pathways. In this review, we summarize the available information on regulating factors and the mechanisms of GFNs toxicity, and propose some challenges and suggestions for further investigations of GFNs, with the aim of completing the toxicology mechanisms, and providing suggestions to improve the biological safety of GFNs and facilitate their wide application.

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“…synthesized graphene quantum dots (GQDs) with an average diameter of 8 nm, which have excellent photoluminescence properties, low cytotoxicity and great bio‐compatibility. Most importantly, GQDs exhibited an excellent inhibitory effect on the aggregation of Aβ42 peptides . They further covalent bound GQDs with tramiprosate to increase the binding sites and enlarge steric hindrance between neighboring Aβ42 peptides .…”

Section: Resultsmentioning

confidence: 99%

Black Phosphorus Nanomaterials Regulate the Aggregation of Amyloid‐β

Lim

Zhou

et al. 2019

ChemNanoMat

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Aggregation of amyloid‐β (Aβ) plays important roles in the progression of Alzheimer's disease (AD), and various carbon‐based nanomaterials have been shown to significantly inhibit aggregation of Aβ. A new member of the family of two‐dimensional (2D) nanomaterials, black phosphorus (BP), has been successfully prepared. Compared to other nanomaterials, BP has a higher surface‐to‐volume ratio, so it has strong adsorption ability for Aβ, and can thereby regulate the aggregation of Aβ. Herein, black phosphorus (BP) nanomaterials are proposed to regulate the aggregation of Aβ for the first time, and the corresponding mechanism is clarified. This work provides new insight into the development of BP‐based strategies to prevent amyloidosis.

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Graphene quantum dots for the inhibition of β amyloid aggregation

Cited by 137 publications

References 49 publications

Graphene oxide and reduced graphene oxide induced neural pheochromocytoma-derived PC12 cell lines apoptosis and cell cycle alterations via the ERK signaling pathways

Graphene oxide and reduced graphene oxide induced neural pheochromocytoma-derived PC12 cell lines apoptosis and cell cycle alterations via the ERK signaling pathways

Toxicity of graphene-family nanoparticles: a general review of the origins and mechanisms

Black Phosphorus Nanomaterials Regulate the Aggregation of Amyloid‐β

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