A primary culture system of adult rat heart cells for the evaluation of cocaine toxicity

Welder, Allison A.

doi:10.1016/0300-483x(92)90111-q

Cited by 48 publications

(26 citation statements)

References 15 publications

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“…The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT, Sigma, USA) assay was used to measure cell viability [39]. The principle of this assay is that mitochondrial dehydrogenase in viable cells reduces MTT to a blue formazan.…”

Section: Mtt Assay For Cell Viabilitymentioning

confidence: 99%

Cholestin (Monascus purpureus rice) inhibits homocysteine-induced reactive oxygen species generation, nuclear factor-κB activation, and vascular cell adhesion molecule-1 expression in human aortic endothelial cells

Lin

Chen

et al. 2007

J Biomed Sci

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Hyperhomocysteinemia is associated with dysfunction and an independent risk factor of cardiovascular diseases. Cholestin (Monascus purpureus-fermented rice), contains a naturally-occurring statin, which has lipid-modulating and anti-inflammatory effects. We investigated the effects of Cholestin extract on the expression of vascular cell adhesion molecule-1 (VCAM-1) by homocysteine (HCY)-treated human aortic endothelial cells (HAECs). Supplement of HAECs with Cholestin extract significantly suppressed cellular binding between the human monocytic cells U937 and HCY-stimulated HAECs. Quantitative PCR and immunoblot analysis showed that Cholestin extract significantly attenuated HCY-induced expression of VCAM-1 mRNA and protein, respectively. Gel shift assays showed that Cholestin treatment reduced HCY-activated transcription factor nuclear factor-kappaB (NF-kappaB). Furthermore, Cholestin also attenuated reactive oxygen species (ROS) generation in vitro and in HCY-treated HAECs. Supplement with statins including simvastatin and parastatin gave similar results as compared with Cholestin. In conclusion, Cholestin reduces HCY-stimulated endothelial adhesiveness as well as downregulating intracellular ROS formation, NF-kappaB activation, and VCAM-1 expression in HAECs, supporting the notion that the natural compound Cholestin may have potential implications in clinical atherosclerosis disease.

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Section: Mtt Assay For Cell Viabilitymentioning

confidence: 99%

Cholestin (Monascus purpureus rice) inhibits homocysteine-induced reactive oxygen species generation, nuclear factor-κB activation, and vascular cell adhesion molecule-1 expression in human aortic endothelial cells

Lin

Chen

et al. 2007

J Biomed Sci

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“…Cell Viability Assay Using MTT The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay 10) was used to measure cell viability. Briefly, endothelial cells were seeded onto 96-well culture plate at a density 5ϫ10 4 of cornuside (1ϫ10…”

Section: Plant Materials and Isolation Of Cornusidementioning

confidence: 99%

Cornuside Suppresses Cytokine-Induced Proinflammatory and Adhesion Molecules in the Human Umbilical Vein Endothelial Cells

Kang

Moon

Lee

et al. 2007

Biological & Pharmaceutical Bulletin

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Cornuside is a bisiridoid glucoside compound isolated from the fruit of Cornus officinalis SIEB. et ZUCC. The present study was designed to examine the effects of cornuside on expression levels of cytokine-induced proinflammatory and adhesion molecules in the human umbilical vein endothelial cells (HUVECs). Cornuside treatment attenuated tumor necrosis factor-a a (TNF-a a)-induced nuclear factor-kappa B (NF-k kB) p65 translocation in HUVECs. In addition, cornuside suppressed the expression levels of endothelial cell adhesion molecules including intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) induced by TNF-a a. TNF-a a-induced monocyte chemoattractant protein 1 (MCP-1) expression was also attenuated by treatment of cornuside. These inhibitory effects of cornuside on proinflammatory and adhesion molecules were not due to decreased HUVEC viability as assessed by MTT test. Taken together, the present study suggests that cornuside suppresses expression levels of cytokine-induced proinflammatory and adhesion molecules in the human endothelial cells.

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“…Mitochondrial dehydrogenase activity was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay described by Welder [1992]. After washes with PBS, 500 ml of MTT medium (0.5 mg/ml MTT in culture medium) was added to each well and reacted for 4 h at 378C in a CO 2 incubator.…”

Section: Measurement Of Cytotoxicitymentioning

confidence: 99%

Signaling pathway of magnolol‐stimulated lipolysis in sterol ester‐loaded 3T3‐L1 preadipocyes

Huang

Shen

Yeo

et al. 2004

J of Cellular Biochemistry

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The aims of the present study were to examine the effect of magnolol on lipolysis in sterol ester (SE)-loaded 3T3-L1 preadipocytes and to determine the signaling mechanism involved. We demonstrate that magnolol treatment resulted in a decreased number and surface area of lipid droplets, accompanied by release of glycerol. The lipolytic effect of magnolol was not mediated by PKA based on the facts that magnolol did not induce an elevation of intracellular cAMP levels, and protein kinase A (PKA) inhibitor KT5720 did not block magnolol-induced lipolysis. Calcium/calmodulin-dependent protein kinase (CaMK) was involved in this signaling pathway, since magnolol-induced a transient rise of intracellular [Ca(2+)] and Ca(2+) influx across the plasma membrane, and CaMK inhibitor significantly abolished magnolol-induced lipolysis. Moreover, magnolol increased the relative levels of phosphorylated extracellular signal-related kinases (ERK1 and ERK2). In support of the involvement ERK, we demonstrated that magnolol-induced lipolysis was inhibited by PD98059, an inhibitor of mitogen-activated protein kinase kinase (MEK), and PD98059 reversed magnolol-induced ERK phosphorylation. Further, the relationship between CaMK and ERK was connected by the finding that CaMK inhibitor also blocked magnolol-induced ERK phosphorylation. Taken together, these findings suggest that magnolol-induced lipolysis is both CaMK- and ERK-dependent, and this lipolysis signaling pathway is distinct from the traditional PKA pathway. ERK phosphorylation is reported to enhance lipolysis by direct activation of hormone sensitive lipase (HSL), thus magnolol may likely activate HSL through ERK and increase lipolysis of adipocytes.

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A primary culture system of adult rat heart cells for the evaluation of cocaine toxicity

Cited by 48 publications

References 15 publications

Cholestin (Monascus purpureus rice) inhibits homocysteine-induced reactive oxygen species generation, nuclear factor-κB activation, and vascular cell adhesion molecule-1 expression in human aortic endothelial cells

Cholestin (Monascus purpureus rice) inhibits homocysteine-induced reactive oxygen species generation, nuclear factor-κB activation, and vascular cell adhesion molecule-1 expression in human aortic endothelial cells

Cornuside Suppresses Cytokine-Induced Proinflammatory and Adhesion Molecules in the Human Umbilical Vein Endothelial Cells

Signaling pathway of magnolol‐stimulated lipolysis in sterol ester‐loaded 3T3‐L1 preadipocyes

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