Oxidative modulation of marcaine and lekoptin in H9C2 rat myoblasts

Kulbacka, Julita; Bar, Julita; Chwiłkowska, Agnieszka; Dumańska, Małgorzata; Drąg-Zalesińska, Małgorzata; Wysocka, Teresa; Stach, Kamilla; Bednarz, Iwona; Ługowski, Mateusz; Marcinkowska, Anna; Gamian, Andrzej; Saczko, Jolanta

doi:10.1038/aps.2008.27

Cited by 4 publications

(10 citation statements)

References 33 publications

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“…These results support the hypothesis that the mitochondria are critical in cellular apoptosis. Furthermore, mitochondria have been implicated in the generation of ROS (37). These previous results are concordant with the results of the present study, and suggest that BPV-induced toxicity directly affects mitochondrial survival.…”

Section: A B C Dsupporting

confidence: 93%

Rescue effect of lipid emulsion on bupivacaine-induced cardiac toxicity in cardiomyocytes

Yang

Bai

et al. 2015

Molecular Medicine Reports

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The aim of the present study was to investigate the mechanism underlying the rescue effect of lipid emulsion on bupivacaine (BPV)‑induced cardiomyocyte toxicity. The inhibitory effects of BPV on H9c2 myoblast cell proliferation were investigated using an MTT assay. The H9c2 myoblast cells were treated with either 1 mM BPV or 1% lipid emulsion (LE) alone, or co‑treated with both of the drugs. Cell apoptosis was detected using both Annexin V/propidium iodide staining and a terminal deoxynucleotidyl transferase dUTP assay. The protein expression levels of apoptosis-associated proteins were quantified using western blot analysis, and the mRNA expression levels were quantified by reverse transcription‑quantitative polymerase chain reaction. The expression levels of reactive oxidative species, malondialdehyde, superoxide dismutase, and catalase were quantified using the optical density values obtained from a spectrophotometer. In addition, the mechanism underlying the mitochondrial function of the H9c2 myoblast cells was investigated using both JC‑1 staining, and cyclosporin A and atractyloside treatment. The results indicated that the H9c2 myoblast cells treated with BPV exhibited significantly higher levels of apoptosis. Furthermore, BPV treatment increased the levels of oxidative stress, and caused mitochondrial dysfunction within the H9c2 myoblast cells. LE treatment reversed the effects of BPV treatment in the H9c2 myoblast cells.

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Section: A B C Dsupporting

confidence: 93%

Rescue effect of lipid emulsion on bupivacaine-induced cardiac toxicity in cardiomyocytes

Yang

Bai

et al. 2015

Molecular Medicine Reports

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“…Local anesthetics, including BPV, induce decreased cell viability via apoptosis in neuron, myocyte, and H9c2 cells. 7,10 In addition, local anesthetics, including BPV, tetracaine, and lidocaine, attenuate cancer cell proliferation via apoptosis. 8 The cellular signaling pathways responsible for apoptosis are divided into the intrinsic and extrinsic pathways that are associated with mitochondrial stress and the death receptor, respectively.…”

Section: Discussionmentioning

confidence: 99%

“…9 BPV induces apoptosis in H9c2 cells. 10 The local anesthetic cocaine induces apoptosis in fetal myocardial cells. 11 BPV produces a myotoxic effect, leading to myonecrosis.…”

Section: Introductionmentioning

confidence: 99%

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Lipid emulsion attenuates apoptosis induced by a toxic dose of bupivacaine in H9c2 rat cardiomyoblast cells

et al. 2016

Hum Exp Toxicol

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The goal of this in vitro study was to investigate the effect of lipid emulsion on apoptosis induced by a toxic dose of bupivacaine (BPV) in H9c2 rat cardiomyoblast cell lines. The effect of lipid emulsion on the decreased cell viability and count induced by BPV or mepivacaine (MPV) in the H9c2 cells was assessed using an 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide assay or a cell count assay. The effect of BPV or lipid emulsion combined with BPV on cleaved caspase 3, caspase 8, and Bax in H9c2 cells was investigated using Western blotting. A terminal deoxynucleotidyl transferase dUTP2′-deoxyuridine 5′-triphosphate nick end-labeling (TUNEL) assay was performed to detect apoptosis of H9c2 cells treated with BPV alone or lipid emulsion combined with BPV. The magnitude of lipid emulsion-mediated attenuation of decreased cell viability induced by BPV was higher than that of lipid emulsion-mediated attenuation of decreased cell viability induced by MPV. Lipid emulsion attenuated the increases in cleaved caspase 3, caspase 8 and Bax induced by BPV. Lipid emulsion attenuated the increases in TUNEL-positive cells induced by BPV. These results suggest that lipid emulsion attenuates a toxic dose of BPV-induced apoptosis via inhibition of the extrinsic and intrinsic apoptotic pathways. The protective effect of lipid emulsion may be partially associated with the relatively high lipid solubility of BPV.

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“…The final product of cellular fatty-acid peroxidation, malondialdehyde (MDA), was determined according to earlier studies (29,32). The MDA reacts with thiobarbituric acid (TBA) to form a colored complex, TBARS, whose level was measured by the absorbance at a wavelength of 535 nm.…”

Section: Confocal Laser Scanning Microscopy (Clms) Methods Of Cyanine mentioning

confidence: 99%

Photo-oxidative action in MCF-7 cancer cells induced by hydrophobic cyanines loaded in biodegradable microemulsion-templated nanocapsules

et al. 2012

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Abstract. Searching for photodynamic therapy-effective nanocarriers which enable a photosensitizer to be selectively delivered to tumor cells with enhanced bioavailability and diminished dark cytotoxicity is of current interest. We have employed a polymer-based nanoparticle approach to encapsulate the cyanine-type photosensitizer IR-780 in poly(n-butyl cyanoacrylate) (PBCA) nanocapsules. The latter were fabricated by interfacial polymerization in oil-in-water (o/w) microemulsions formed by dicephalic and gemini saccharide-derived surfactants. Nanocarriers were characterized by SEM, AFM and DLS. The efficiency of PBCA nanocapsules as a potential system of photosensitizer delivery to human breast cancer cells was established by dark and photocytotoxicity as the function of the cellular mitochondria. The photodynamic effect of cyanine IR-780 was determined by investigation of oxidative stress markers. The nanocapsules were the main focus of our studies to examine their cellular uptake and dark and photocytotoxicity as the function of the cellular mitochondria as well as oxidative stress markers (i.e., lipid peroxidation and protein damage) in MCF-7/WT cancer cells. The effects of encapsulated IR-780 were compared with those of native photosensitizer. The penetration of the nanocapsules into cancer cells was visualized by CLSM and their uptake was estimated by FACS analysis. Cyanine IR-780 delivered in PBCA nanocapsules to MCF-7/ WT cells retains its sensitivity upon photoirradiation and it is regularly distributed in the cell cytoplasm. The intensity of the photosensitizer-generated oxidative stress depends on IR-780 release from the effective uptake of polymeric nanocapsules and seems to remain dependent upon the surfactant structure in o/w microemulsion-based templates applied to nanocapsule fabrication.

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Oxidative modulation of marcaine and lekoptin in H9C2 rat myoblasts

Cited by 4 publications

References 33 publications

Rescue effect of lipid emulsion on bupivacaine-induced cardiac toxicity in cardiomyocytes

Rescue effect of lipid emulsion on bupivacaine-induced cardiac toxicity in cardiomyocytes

Lipid emulsion attenuates apoptosis induced by a toxic dose of bupivacaine in H9c2 rat cardiomyoblast cells

Photo-oxidative action in MCF-7 cancer cells induced by hydrophobic cyanines loaded in biodegradable microemulsion-templated nanocapsules

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