Cytotoxicity of psammaplin A from a two-sponge association may correlate with the inhibition of DNA replication

Jiang, Yahong; Ahn, Eun-Young; Ryu, Seung Hee; Kim, Dong‐Kyoo; Park, Jang-Su; Yoon, Hwi Joong; You, Song; Lee, Burm−Jong; Lee, Dong Seok; Jung, Jee H.

doi:10.1186/1471-2407-4-70

Cited by 61 publications

(32 citation statements)

References 21 publications

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“…In vitro inhibitory of HaCaT cells is accessed by a CCK-8 toxic assay, which is widely used to evaluate the cytotoxic activity of biomaterials [26]. The inhibitory effect is determined by CCK-8 in the HaCaT cells treated with TiO 2 NPs in the concentration of 10, (Fig.…”

Section: The Inhibitory Effect Of Tio 2 Nps On Hacat Cells By Cck-8 Amentioning

confidence: 99%

In Vitro Toxicity Evaluation of 25-nm Anatase TiO2 Nanoparticles in Immortalized Keratinocyte Cells

Jin

Tang

Guang

et al. 2011

Biol Trace Elem Res

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Titanium dioxide (TiO(2)) nanoparticles (NPs) are massively fabricated and widely used in daily life, and thus potential risk has been posed to human health. However, the mechanism of the interaction between TiO(2) NPs and cells is still unclear. In this study, the interaction of anatase TiO(2) NPs with HaCaT cells is studied in vitro with multi-techniques. The TiO(2) NPs not only insert into cells through endocytic pathway but also penetrate into the cell. The TiO(2) NPs could produce reactive oxygen species (ROS) after dispersion spontaneously. Furthermore, the interaction between TiO(2) NPs and cellular components might also generate ROS. The ROS generation could lead to cellular toxicity if the level of ROS production overwhelms the antioxidant defense. Cytoskeletal components, particularly the microfilaments and microtubules, cause modifications upon exposure to TiO(2) NPs. With all results, the toxicological effects of TiO(2) NPs on HaCaT cell can be simplified into six events.

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Section: The Inhibitory Effect Of Tio 2 Nps On Hacat Cells By Cck-8 Amentioning

confidence: 99%

In Vitro Toxicity Evaluation of 25-nm Anatase TiO2 Nanoparticles in Immortalized Keratinocyte Cells

Jin

Tang

Guang

et al. 2011

Biol Trace Elem Res

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show abstract

“…with an electron carrier, 1-methoxy-5-methylphenazinium, methylsulfate (Cell Counting Kit-8; Dojin Kagaku, Kumamoto, Japan) for 3 h at 37°C, and absorbance was recorded at 450 nm (Jiang et al, 2004). WST-8 was bioreduced by cellular dehydrogenases to an orange formazan product that is soluble in cell culture medium.…”

Section: Retinal Protection By Calpain Inhibitor 381mentioning

confidence: 99%

A Novel Calpain Inhibitor, ((1S)-1-((((1S)-1-Benzyl-3-cyclopropylamino-2,3-di-oxopropyl)amino)carbonyl)-3-methylbutyl)carbamic Acid 5-Methoxy-3-oxapentyl Ester (SNJ-1945), Reduces Murine Retinal Cell Death In Vitro and In Vivo

Shimazawa¹,

Suemori²,

Inokuchi³

et al. 2009

J Pharmacol Exp Ther

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We examined whether ((1S)-1-((((1S)-1-benzyl-3-cyclopropylamino-2,3-di-oxopropyl)amino)carbonyl)-3-methylbutyl)carbamic acid 5-methoxy-3-oxapentyl ester (SNJ-1945), a new orally available calpain inhibitor, might reduce retinal cell death in vivo and/or in vitro. Retinal cell damage was induced in vivo in mice by intravitreal injection of N-methyl-D-aspartate (NMDA), and SNJ-1945 was intraperitoneally or orally administered twice. NMDA-induced calpain activity (measured as the cleaved products of ␣-spectrin) and its substrate, p35 (a neuron-specific activator for cyclin-dependent kinase 5), in the retina were examined by immunoblotting. In RGC-5 (a rat retinal ganglion cell line) cell culture, cell damage was induced by a 4-h oxygenglucose deprivation (OGD) treatment followed by an 18-h reoxygenation period. In mouse retinas, SNJ-1945 (30 or 100 mg/kg i.p., 100 or 200 mg/kg p.o.) significantly inhibited the cell loss in the ganglion cell layer (GCL) and the thinning of the inner plexiform layer induced by NMDA. Furthermore, the number of positive cells for terminal deoxynucleotidyl transferase dUTP nick-end labeling was significantly reduced in the GCL and the inner nuclear layer of retinas treated with SNJ-1945 compared with vehicle-treated retinas 24 h after NMDA injection. Levels of cleaved ␣-spectrin products increased and p35 decreased 6 h after NMDA injection or later, and their effects were attenuated by SNJ-1945. In vitro, SNJ-1945 (10 and 100 M) inhibited the OGD stress-induced reduction in cell viability. In conclusion, SNJ-1945 may afford valuable neuroprotection against retinal diseases, because it was effective against retinal damage both in vitro and in vivo. Our results also indicate that calpain activation and subsequent p35 degradation may be involved in the mechanisms underlying retinal cell death.Retinal ganglion cell (RGC) death is a common feature of many ophthalmic disorders, including glaucoma, optic neuropathies, and various retinovascular diseases (diabetic retinopathy and retinal vein occlusions). Retinal ganglion cells are extremely sensitive to the effects of both glutamate and its analog N-methyl-D-aspartate (NMDA), both of which produce a dosedependent cell loss in vivo and in vitro. In addition, glutamate toxicity has been implicated in the pathophysiology of glaucoma (Dreyer, 1998). Activation of Ca 2ϩ -permeable NMDA receptors and the subsequent neuronal Ca 2ϩ overloading have been shown to mediate glutamate-induced neuron death (Choi, 1994). Induction of the Ca 2ϩ -activated neutral cysteine protease -calpain by micromolar concentrations of Ca 2ϩ occurs early in excitotoxic neuron death (Siman et al., 1989;Faddis et al., 1997). Similar to the caspases, -calpain cleaves a variety of cytoskeletal proteins, enzymes, and transcription factors and could also interfere with the proteolytic activity of the caspases (Croall and DeMartino, 1991).

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“…In this study, the in vitro cytotoxicity of the IC nanoparti- cles was evaluated by a CCK-8 toxic assay, which was widely used for the evaluation of the cytotoxicity of drugs or biomaterials [21]. The experimental design was guided by the CCK-8 technical manual.…”

Section: In Vitro Evaluation Of Ic Nanoparticlesmentioning

confidence: 99%

Study on the α-cyclodextrin/poly(ethylene glycol) self-assembly supramolecular nanoparticles for drug delivery

Wang

et al. 2010

Sci. China Chem.

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This paper reports the synthesis and drug delivery properties of a novel supramolecular nanoparticle. α-Cyclodextrins (α-CD) were threaded on cinnamic acid modified poly(ethylene glycol) to form inclusion complex nanoparticles by supramolecular self-assemble. The anti-tumor drug doxorubicin was loaded in the nanoparticles and released in vitro to study the drug release behavior and the anti-tumor effects. The structure and morphology of the nanoparticles were characterized by nuclear magnetic resonance, X-ray diffraction, ultraviolet absorbance, dynamic laser scattering, scanning electronic microscopy, transmission electron microscopy and atom force microscopy. The distribution of the drug loaded nanoparticles in cells and the anti-tumor effects were studied by confocal laser microscopy. The results demonstrate that the supramolecular nanoparticle is biocompatible and it is a promising carrier for drug delivery systems. supramolecular self-assembly, nanoparticles, drug delivery

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Cytotoxicity of psammaplin A from a two-sponge association may correlate with the inhibition of DNA replication

Cited by 61 publications

References 21 publications

In Vitro Toxicity Evaluation of 25-nm Anatase TiO2 Nanoparticles in Immortalized Keratinocyte Cells

In Vitro Toxicity Evaluation of 25-nm Anatase TiO2 Nanoparticles in Immortalized Keratinocyte Cells

A Novel Calpain Inhibitor, ((1S)-1-((((1S)-1-Benzyl-3-cyclopropylamino-2,3-di-oxopropyl)amino)carbonyl)-3-methylbutyl)carbamic Acid 5-Methoxy-3-oxapentyl Ester (SNJ-1945), Reduces Murine Retinal Cell Death In Vitro and In Vivo

Study on the α-cyclodextrin/poly(ethylene glycol) self-assembly supramolecular nanoparticles for drug delivery

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