Determination of S-carboxymethylcysteine in serum by reversed-phase ion-pair liquid chromatography with column switching following pre-column derivatization with o-phthalaldehyde

Schutter, J.A. De; Weken, G. Van der; Bossche, W. Van den; Moerloose, P. De

doi:10.1016/s0378-4347(00)83921-3

Cited by 19 publications

(6 citation statements)

References 5 publications

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“…Although it should be pointed out that, after the oral ingestion of daily doses of carbocisteine (1500 mg), the peak serum concentration in the serum was 78 μM at 2 h, and mean serum concentration was 4.9 μM at 10 h after ingestion [26]. In some literature reports, the concentrations of 10 μM were chosen to determine the effects of carbocisteine [15,25].…”

Section: Discussionmentioning

confidence: 99%

Carbocisteine attenuates hydrogen peroxide-induced inflammatory injury in A549 cells via NF-κB and ERK1/2 MAPK pathways

Wang

Zheng

Zhu³

et al. 2015

International Immunopharmacology

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Section: Discussionmentioning

confidence: 99%

Carbocisteine attenuates hydrogen peroxide-induced inflammatory injury in A549 cells via NF-κB and ERK1/2 MAPK pathways

Wang

Zheng

Zhu³

et al. 2015

International Immunopharmacology

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“…The cultured human tracheal epithelial cells were treated with L-carbocisteine (10 M) from 3 days before FluA virus infection until the end of the experiments after FluA virus infection (34,37) unless we describe other concentrations or treatment periods. The concentrations of L-carbocisteine (10 M) were chosen because the maximum concentrations of L-carbocisteine in the serum became Ͼ10 M after oral ingestion of 1,500 mg of L-carbocisteine (9).…”

Section: Methodsmentioning

confidence: 99%

Inhibitory effects of carbocisteine on type A seasonal influenza virus infection in human airway epithelial cells

Yamaya

Nishimura²,

Shinya

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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Type A human seasonal influenza (FluA) virus infection causes exacerbations of bronchial asthma and chronic obstructive pulmonary disease (COPD). l-carbocisteine, a mucolytic agent, reduces the frequency of common colds and exacerbations in COPD. However, the inhibitory effects of l-carbocisteine on FluA virus infection are uncertain. We studied the effects of l-carbocisteine on FluA virus infection in airway epithelial cells. Human tracheal epithelial cells were pretreated with l-carbocisteine and infected with FluA virus (H(3)N(2)). Viral titers in supernatant fluids, RNA of FluA virus in the cells, and concentrations of proinflammatory cytokines in supernatant fluids, including IL-6, increased with time after infection. l-carbocisteine reduced viral titers in supernatant fluids, RNA of FluA virus in the cells, the susceptibility to FluA virus infection, and concentrations of cytokines induced by virus infection. The epithelial cells expressed sialic acid with an alpha2,6-linkage (SAalpha2,6Gal), a receptor for human influenza virus on the cells, and l-carbocisteine reduced the expression of SAalpha2,6Gal. l-carbocisteine reduced the number of acidic endosomes from which FluA viral RNA enters into the cytoplasm and reduced the fluorescence intensity from acidic endosomes. Furthermore, l-carbocisteine reduced NF-kappaB proteins including p50 and p65 in the nuclear extracts of the cells. These findings suggest that l-carbocisteine may inhibit FluA virus infection, partly through the reduced expression of the receptor for human influenza virus in the human airway epithelial cells via the inhibition of NF-kappaB and through increasing pH in endosomes. l-carbocisteine may reduce airway inflammation in influenza virus infection.

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“…This timeframe was chosen because the maximum concentrations of SCMC in the serum become .10 mM after oral ingestion of 1,500 mg SCMC [25]. The cells were then exposed to RV2 (1610 5 TCID50?mL -1 ), RV14 (1610 5 TCID50?mL -1 ) or vehicle (Eagle's minimum essential medium) for 60 min and cultured at 33uC with rolling, as described previously [7,17].…”

Section: Effects Of Carbocisteine On Viral Infectionmentioning

confidence: 99%

Carbocisteine inhibits rhinovirus infection in human tracheal epithelial cells

Yasuda

Yamaya²,

Sasaki³

et al. 2006

Eur Respir J

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The aim of the study was to examine the effects of a mucolytic drug, carbocisteine, on rhinovirus (RV) infection in the airways.Human tracheal epithelial cells were infected with a major-group RV, RV14. RV14 infection increased virus titres and the cytokine content of supernatants. Carbocisteine reduced supernatant virus titres, the amount of RV14 RNA in cells, cell susceptibility to RV infection and supernatant cytokine concentrations, including interleukin (IL)-6 and IL-8, after RV14 infection. Carbocisteine reduced the expression of mRNA encoding intercellular adhesion molecule (ICAM)-1, the receptor for the major group of RVs. It also reduced the supernatant concentration of a soluble form of ICAM-1, the number and fluorescence intensity of acidic endosomes in the cells before RV infection, and nuclear factor-kB activation by RV14. Carbocisteine also reduced the supernatant virus titres of the minor group RV, RV2, although carbocisteine did not reduce the expression of mRNA encoding a low density lipoprotein receptor, the receptor for RV2.These results suggest that carbocisteine inhibits rhinovirus 2 infection by blocking rhinovirus RNA entry into the endosomes, and inhibits rhinovirus 14 infection by the same mechanism as well as by reducing intercellular adhesion molecule-1 levels. Carbocisteine may modulate airway inflammation by reducing the production of cytokines in rhinovirus infection.

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Determination of S-carboxymethylcysteine in serum by reversed-phase ion-pair liquid chromatography with column switching following pre-column derivatization with o-phthalaldehyde

Cited by 19 publications

References 5 publications

Carbocisteine attenuates hydrogen peroxide-induced inflammatory injury in A549 cells via NF-κB and ERK1/2 MAPK pathways

Carbocisteine attenuates hydrogen peroxide-induced inflammatory injury in A549 cells via NF-κB and ERK1/2 MAPK pathways

Inhibitory effects of carbocisteine on type A seasonal influenza virus infection in human airway epithelial cells

Carbocisteine inhibits rhinovirus infection in human tracheal epithelial cells

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