The Experts below are selected from a list of 381 Experts worldwide ranked by ideXlab platform
Yuji Ishibashi - One of the best experts on this subject based on the ideXlab platform.
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Expression and role of sugar chains on airway mucus during the exacerbation of airway inflammation
Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan, 2012Co-Authors: Yuji Ishibashi, Yoshio Inouye, Akiyoshi TaniguchiAbstract:Human bronchial mucins, such as MUC5AC, have traditionally been defined as a family of high-molecular weight glycoproteins. Changes in the contents of sugar chains on MUC5AC are among the fundamental features in inflammatory respiratory disease. The changes have been shown to lead to unfavorable alterations in the viscosity of mucus, resulting in impairment of mucociliary transport, vulnerability to viral/bacterial infection as sugar chains play an important role in adhesion of some viruses and bacteria to the epithelium, and finally inflammatory cell infiltration in the airway. Recently, we found that expression of some glycosyltransferases associated with the contents and structure of sugar chains is regulated by phosphatidylinositol-phospholipase (PI-PL) C signaling in cells. L-Carbocisteine, a mucoregulatory drug, normalized or balanced fucosylated and sialylated sugar chains, such as sialyl Lewis x through inhibition of PI-PL C signaling. We prepared MUC5AC fusion protein with tandem repeats associated with MUC5AC, and confirmed that L-Carbocisteine inhibited the increases in viscosity associated with sialyl Lewis x expression levels. In addition, the clinical study (2008) noted that L-Carbocisteine reduced the frequency of common colds and exacerbation of symptoms in patients with COPD. These favorable effects in patients may be due to normalization of sugar chain contents on mucins. We suggest that the inhibitory effect on infection of airway epithelial cells by rhinoviruses, respiratory syncytial virus, and influenza viruses by treatment with L-Carbocisteine may also be based on the regulation of sugar chain contents or structures on mucins.
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Carbocisteine promotes phagocytosis of apoptotic cells by alveolar macrophages.
European journal of pharmacology, 2011Co-Authors: Masako Inoue, Hisashi Nogawa, Yuji Ishibashi, Tokutaro YasueAbstract:Clearance of apoptotic cells, so-called efferocytosis, by alveolar macrophages (AMs) is important for lung homeostasis and is impaired in pulmonary inflammatory diseases, such as chronic obstructive pulmonary disease and asthma. Carbocisteine, a mucoregulatory drug, corrects the contents of fucose in airway mucus and has anti-inflammatory properties in airway inflammation. Thus, we conducted the present study to better understand the anti-inflammatory properties of Carbocisteine. First, we induced airway inflammation in mice with lipopolysaccharide intratracheally. Carbocisteine significantly decreased neutrophil numbers in bronchoalveolar lavage fluid at the resolution phase of inflammation, implying the promotion of neutrophil clearance. Then, we investigated whether Carbocisteine would enhance the efferocytosis by AMs isolated from mice and found that this drug promoted not only the phagocytosis but also the binding of apoptotic cells to AMs in vitro. Furthermore, Carbocisteine decreased the fucose residues stained with fluorescent fucose-binding lectin, Lens culinaris agglutinin, on the cell surface of AMs. We found here that removing fucose residues from cell surfaces of AMs by fucosidase markedly enhanced both the binding and phagocytosis of apoptotic cells. Finally, AMs from mice orally given Carbocisteine also promoted both the binding and phagocytosis ex vivo similarly to in vitro. These results suggest that Carbocisteine could promote the clearance of apoptotic cells by AMs in airway. In addition, the present findings suggest that the binding and phagocytosis of apoptotic cells may be modulated by fucose residues on the cell surface of AMs.
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Carbocisteine normalizes the viscous property of mucus through regulation of fucosylated and sialylated sugar chain on airway mucins.
European Journal of Pharmacology, 2010Co-Authors: Yuji Ishibashi, Goh Takayama, Yoshio Inouye, Akiyoshi TaniguchiAbstract:Abstract Almost all of fucose and sialic acid in mucus are found on the mucus glycoproteins (mucins), and these sugar components on mucins are known to be associated with the viscous property of mucus. We have reported some aspects of Carbocisteine, a mucoregulatory drug, correcting fucose and sialic acid contents in mucus. At present, Carbocisteine's expectorant action of airway mucus is postulated to involve — the regulation of fucose and sialic acid contents on mucins. However little information is available about the relationship between the viscosity and sugar contents on mucins when treated with Carbocisteine. To investigate further the mechanism behind the action of Carbocisteine, the present study prepared MUC5AC fusion protein which has tandem repeat regions associated with MUC5AC, and evaluated the effects of Carbocisteine on tumor necrosis factor (TNF)-α-induced increases of mucus viscosity and sialyl-Lewis x-epitopes antigen, an antigen which consists of fucosylated and sialylated sugar chains on the MUC5AC fusion proteins. Carbocisteine inhibited the TNF-α-induced increases of the viscosity and sialyl-Lewis x-epitopes on MUC5AC fusion protein. These findings suggest that Carbocisteine may normalize the viscosity of mucus through “balancing” of fucose and sialic acid contents on airway mucins.
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Carbocisteine can scavenge reactive oxygen species in vitro
Respirology, 2009Co-Authors: Hisashi Nogawa, Yuji Ishibashi, Akitsu Ogawa, Kayoko Masuda, Takeshi Tsubuki, Tomoko Kameda, Shigeki MatsuzawaAbstract:BACKGROUND AND OBJECTIVE Reactive oxygen species (ROS) play an important role in the pathogenesis of various respiratory diseases. Carbocisteine, a mucoregulatory drug, is used in the treatment of several disease states but little information is available about its scavenger effects on ROS. The present study was designed to examine the scavenger effects of Carbocisteine on ROS. METHODS The oxidation-reduction potential of Carbocisteine was measured, and its scavenger effects on hypochlorous acid (HOCl), hydrogen peroxide (H(2)O(2)), hydroxyl radical (OH(*)) and peroxynitrite (ONOO(-)) were examined in cell-free conditions. The effects of Carbocisteine on ROS generated from rat neutrophils, intracellular oxidative stress and release of inflammatory cytokines (IL-8 and IL-6) from IL-1 beta-induced airway epithelial cells, NCI-H292 cells, were investigated. RESULTS Carbocisteine provided a reducing stage and showed scavenger effects on H(2)O(2), HOCl, OH(*) and ONOO(-) in cell-free conditions. Carbocisteine inhibited ROS generation from rat neutrophils, intracellular oxidative stress and release of IL-8 and IL-6 from NCI-H292 cells. N-acetyl-L-cysteine, a radical scavenger, also inhibited these events related to ROS as well as Carbocisteine. CONCLUSIONS These results suggest that Carbocisteine could exert anti-inflammatory and anti-oxidant effects through directly scavenging ROS in addition to its previously known mucoregulatory effect.
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Effects of Carbocisteine on sialyl-Lewis x expression in an airway carcinoma cell line stimulated with tumor necrosis factor-α
European journal of pharmacology, 2006Co-Authors: Yuji Ishibashi, Yoshio Inouye, Shigeru Imai, Teruo Okano, Akiyoshi TaniguchiAbstract:Carbocisteine is a mucoregulatory drug normalizing sialic acid and fucose contents in mucins through the regulation of glycosyltransferase activities. Tumor necrosis factor (TNF)-alpha-induced overexpression of sialyl-Lewis x epitopes, containing sialic acid and fucose, in mucins were previously reported to be regulated by glycosyltransferase mRNAs expression through phosphatidyl inositol-specific phospholipase C (PI-PLC) signaling pathways [Ishibashi, Y., Inouye, Y., Okano, T., Taniguchi, A., 2005. Regulation of sialyl-Lewis x epitope expression by TNF-alpha and EGF in an airway carcinoma cell line. Glycoconj. J. 22, 53-62]. To investigate the mechanism behind the mucoregulatory action of Carbocisteine, the present study evaluated the effects of Carbocisteine on TNF-alpha-induced overexpression of sialyl-Lewis x epitopes in NCI-H292 cells. 100 mug/ml of Carbocisteine was able to inhibit the TNF-alpha-induced expression of hST3GallV mRNA, FUT3 mRNA, C2/4GnT mRNA and sialyl-Lewis x epitopes as well as the TNF-alpha-induced activity of PI-PLC in NCI-H292 cells. These findings suggest that Carbocisteine may normalize the sialyl-Lewis x epitopes expression in mucins through the inhibition of cellular PI-PLC activity in vivo.
Akiyoshi Taniguchi - One of the best experts on this subject based on the ideXlab platform.
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Expression and role of sugar chains on airway mucus during the exacerbation of airway inflammation
Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan, 2012Co-Authors: Yuji Ishibashi, Yoshio Inouye, Akiyoshi TaniguchiAbstract:Human bronchial mucins, such as MUC5AC, have traditionally been defined as a family of high-molecular weight glycoproteins. Changes in the contents of sugar chains on MUC5AC are among the fundamental features in inflammatory respiratory disease. The changes have been shown to lead to unfavorable alterations in the viscosity of mucus, resulting in impairment of mucociliary transport, vulnerability to viral/bacterial infection as sugar chains play an important role in adhesion of some viruses and bacteria to the epithelium, and finally inflammatory cell infiltration in the airway. Recently, we found that expression of some glycosyltransferases associated with the contents and structure of sugar chains is regulated by phosphatidylinositol-phospholipase (PI-PL) C signaling in cells. L-Carbocisteine, a mucoregulatory drug, normalized or balanced fucosylated and sialylated sugar chains, such as sialyl Lewis x through inhibition of PI-PL C signaling. We prepared MUC5AC fusion protein with tandem repeats associated with MUC5AC, and confirmed that L-Carbocisteine inhibited the increases in viscosity associated with sialyl Lewis x expression levels. In addition, the clinical study (2008) noted that L-Carbocisteine reduced the frequency of common colds and exacerbation of symptoms in patients with COPD. These favorable effects in patients may be due to normalization of sugar chain contents on mucins. We suggest that the inhibitory effect on infection of airway epithelial cells by rhinoviruses, respiratory syncytial virus, and influenza viruses by treatment with L-Carbocisteine may also be based on the regulation of sugar chain contents or structures on mucins.
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Carbocisteine normalizes the viscous property of mucus through regulation of fucosylated and sialylated sugar chain on airway mucins.
European Journal of Pharmacology, 2010Co-Authors: Yuji Ishibashi, Goh Takayama, Yoshio Inouye, Akiyoshi TaniguchiAbstract:Abstract Almost all of fucose and sialic acid in mucus are found on the mucus glycoproteins (mucins), and these sugar components on mucins are known to be associated with the viscous property of mucus. We have reported some aspects of Carbocisteine, a mucoregulatory drug, correcting fucose and sialic acid contents in mucus. At present, Carbocisteine's expectorant action of airway mucus is postulated to involve — the regulation of fucose and sialic acid contents on mucins. However little information is available about the relationship between the viscosity and sugar contents on mucins when treated with Carbocisteine. To investigate further the mechanism behind the action of Carbocisteine, the present study prepared MUC5AC fusion protein which has tandem repeat regions associated with MUC5AC, and evaluated the effects of Carbocisteine on tumor necrosis factor (TNF)-α-induced increases of mucus viscosity and sialyl-Lewis x-epitopes antigen, an antigen which consists of fucosylated and sialylated sugar chains on the MUC5AC fusion proteins. Carbocisteine inhibited the TNF-α-induced increases of the viscosity and sialyl-Lewis x-epitopes on MUC5AC fusion protein. These findings suggest that Carbocisteine may normalize the viscosity of mucus through “balancing” of fucose and sialic acid contents on airway mucins.
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Effects of Carbocisteine on sialyl-Lewis x expression in an airway carcinoma cell line stimulated with tumor necrosis factor-α
European journal of pharmacology, 2006Co-Authors: Yuji Ishibashi, Yoshio Inouye, Shigeru Imai, Teruo Okano, Akiyoshi TaniguchiAbstract:Carbocisteine is a mucoregulatory drug normalizing sialic acid and fucose contents in mucins through the regulation of glycosyltransferase activities. Tumor necrosis factor (TNF)-alpha-induced overexpression of sialyl-Lewis x epitopes, containing sialic acid and fucose, in mucins were previously reported to be regulated by glycosyltransferase mRNAs expression through phosphatidyl inositol-specific phospholipase C (PI-PLC) signaling pathways [Ishibashi, Y., Inouye, Y., Okano, T., Taniguchi, A., 2005. Regulation of sialyl-Lewis x epitope expression by TNF-alpha and EGF in an airway carcinoma cell line. Glycoconj. J. 22, 53-62]. To investigate the mechanism behind the mucoregulatory action of Carbocisteine, the present study evaluated the effects of Carbocisteine on TNF-alpha-induced overexpression of sialyl-Lewis x epitopes in NCI-H292 cells. 100 mug/ml of Carbocisteine was able to inhibit the TNF-alpha-induced expression of hST3GallV mRNA, FUT3 mRNA, C2/4GnT mRNA and sialyl-Lewis x epitopes as well as the TNF-alpha-induced activity of PI-PLC in NCI-H292 cells. These findings suggest that Carbocisteine may normalize the sialyl-Lewis x epitopes expression in mucins through the inhibition of cellular PI-PLC activity in vivo.
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Effects of Carbocisteine on altered activities of glycosidase and glycosyltransferase and expression of Muc5ac in SO2-exposed rats.
European journal of pharmacology, 2004Co-Authors: Yuji Ishibashi, Akiyoshi Taniguchi, Fumiyoshi Kobayashi, Akira Idesawa, Shigeki MatsuzawaAbstract:Carbocisteine is a mucoregulatory drug regulating fucose and sialic acid contents in mucus glycoprotein. To investigate the mechanism of Carbocisteine action, we evaluated the effects of Carbocisteine on the activity of fucosidase, sialidase, fucosyltransferase and sialyltransferase, and on the expression of Muc5ac mRNA in the airway epithelium of SO(2)-exposed rats. Wistar rats were repeatedly exposed to a 300-ppm SO(2) gas for 44 days. Carbocisteine (125 and 250 mg/kg x2/day) was administered for 25 days after 20 days of SO(2) gas exposure. These enzyme activities were measured by fluorogenic substrate or glycoproteinic exogenous acceptor method. The expression levels of Muc5ac mRNA and protein were determined with real-time reverse transcriptase-polymerase chain reaction (real-time RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Carbocisteine (250 mg/kg x2/day) inhibited all the changes in these enzyme activities and the expressions of Muc5ac mRNA and protein in the lung after repeated SO(2) exposure. These findings suggest that Carbocisteine may normalize fucose and sialic acid contents in mucin glycoprotein through regulation of these enzyme activities, and inhibition of both Muc5ac mRNA and protein expressions in SO(2)-exposed rats.
Mutsuo Yamaya - One of the best experts on this subject based on the ideXlab platform.
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Increased rhinovirus replication in nasal mucosa cells in allergic subjects is associated with increased ICAM-1 levels and endosomal acidification and is inhibited by L-Carbocisteine.
Immunity inflammation and disease, 2016Co-Authors: Mutsuo Yamaya, Hiroshi Kubo, Hidekazu Nishimura, Ryoichi Nagatomi, Kazuhiro Nomura, Kazuya Arakawa, Nadine Lusamba Kalonji, Tetsuaki KawaseAbstract:Increased viral replication and cytokine production may be associated with the pathogenesis of asthma attacks in rhinovirus (RV) infections. However, the association between increased RV replication and enhanced expression of intercellular adhesion molecule-1 (ICAM-1), a receptor for a major RV group, in airway epithelial cells has remained unclear. Furthermore, the inhibitory effects of mucolytics, which have clinical benefits in asthmatic subjects, are uncertain. Human nasal epithelial (HNE) cells were infected with type 14 rhinovirus (RV14), a major RV group. RV14 titers and cytokine concentrations, including interleukin (IL)-6 and IL-8, in supernatants, RV14 RNA replication and susceptibility to RV14 infection were higher in HNE cells obtained from subjects in the allergic group (allergic subjects) than in those from subjects in the non-allergic group (non-allergic subjects). ICAM-1 expression and the number and fluorescence intensity of acidic endosomes from which RV14 RNA enters the cytoplasm were higher in HNE cells from allergic subjects, though substantial amounts of interferon (IFN)-γ and IFN-λ were not detected in the supernatant. The abundance of p50 and p65 subunits of transcription factor nuclear factor kappa B (NF-κB) in nuclear extracts of the cells from allergic subjects was higher compared to non-allergic subjects, and an inhibitor of NF-κB, caffeic acid phenethyl ester, reduced the fluorescence intensity of acidic endosomes as well as RV titers and RNA. Furthermore, a mucolytic agent, L-Carbocisteine, reduced RV14 titers and RNA levels, cytokine release, ICAM-1 expression, the fluorescence intensity of acidic endosomes, and NF-κB activation. The increased RV14 replication observed in HNE cells from allergic subjects might be partly associated with enhanced ICAM-1 expression and decreased endosomal pH through NF-κB activation. L-Carbocisteine inhibits RV14 infection by reducing ICAM-1 and acidic endosomes and may, therefore, modulate airway inflammation caused by RV infection in allergic subjects.
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l-Carbocisteine inhibits respiratory syncytial virus infection in human tracheal epithelial cells
Respiratory physiology & neurobiology, 2011Co-Authors: Masanori Asada, Motoki Yoshida, Hiroyasu Yasuda, Hiroshi Kubo, Hidekazu Nishimura, Yukimasa Hatachi, Takahiko Sasaki, Xue Deng, Ryoichi Nagatomi, Mutsuo YamayaAbstract:To examine the effects of l-Carbocisteine on airway infection with respiratory syncytial (RS) virus, human tracheal epithelial cells were pretreated with l-Carbocisteine and infected with RS virus. Viral titer, virus RNA, and pro-inflammatory cytokine secretion, including interleukin (IL)-1 and IL-6, increased with time after infection. l-Carbocisteine reduced the viral titer in the supernatant fluids, the amount of RS virus RNA, RS virus infection susceptibility, and the concentration of pro-inflammatory cytokines induced by virus infection. l-Carbocisteine reduced the expression of intercellular adhesion molecule (ICAM)-1, an RS virus receptor, on the cells. However, l-Carbocisteine had no effects on the expression of heparan sulfate, a glycosaminoglycan that binds to the RS virus attachment protein, or on the amount of intracellular activated-RhoA, isoform A of the Ras-homologous family, that binds to the RS virus fusion protein. These findings suggest that l-Carbocisteine may inhibit RS virus infection by reducing the expression of ICAM-1. It may also modulate airway inflammation during RS virus infection.
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Inhibitory effects of Carbocisteine on type A seasonal influenza virus infection in human airway epithelial cells
American journal of physiology. Lung cellular and molecular physiology, 2010Co-Authors: Mutsuo Yamaya, Motoki Yoshida, Hiroyasu Yasuda, Hidekazu Nishimura, Kyoko Shinya, Yukimasa Hatachi, Takahiko Sasaki, Masanori Asada, Naoya Fujino, Takaya SuzukiAbstract: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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Carbocisteine inhibits oxidant-induced apoptosis in cultured human airway epithelial cells.
Respirology (Carlton Vic.), 2009Co-Authors: Motoki Yoshida, Katsutoshi Nakayama, Hiroyasu Yasuda, Hiroshi Kubo, Kazuyoshi Kuwano, Hiroyuki Arai, Mutsuo YamayaAbstract:Background and objective: Increased oxidant levels have been associated with exacerbations of COPD, and L-Carbocisteine, a mucolytic agent, reduces the frequency of exacerbations. The mechanisms underlying the inhibitory effects of L-Carbocisteine on oxidant-induced COPD exacerbations were examined in an in vitro study of human airway epithelial cells. Methods: In order to examine the antioxidant effects of L-Carbocisteine, human tracheal epithelial cells were treated with L-Carbocisteine and exposed to hydrogen peroxide (H2O2). Cell apoptosis was assessed using a cell death detection ELISA, and the pathways leading to cell apoptosis were examined by measurement of caspase-3 and caspase-9 by western blot analysis with fluorescent detection. Results: The proportion of apoptotic cells in human tracheal epithelium was increased in a concentration- and time-dependent manner, following exposure to H2O2. Treatment with L-Carbocisteine reduced the proportion of apoptotic cells. In contrast, H2O2 did not increase the concentration of LDH in supernatants of epithelial cells. Exposure to H2O2 activated caspase-3 and caspase-9, and L-Carbocisteine inhibited the H2O2-induced activation of these caspases. L-Carbocisteine activated Akt phosphorylation, which modulates caspase activation, and the inhibitors of Akt, LY294002 and wortmannin, significantly reversed the inhibitory effects of L-Carbocisteine on H2O2-induced cell apoptosis. Conclusions: These findings suggest that in human airway epithelium, L-Carbocisteine may inhibit cell damage induced by H2O2 through the activation of Akt phosphorylation. L-Carbocisteine may have antioxidant effects, as well as mucolytic activity, in inflamed airways.
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L-Carbocisteine reduces neutrophil elastase-induced mucin production.
Respiratory physiology & neurobiology, 2009Co-Authors: Masanori Yasuo, Hiroshi Kubo, Mutsuo Yamaya, Keisaku Fujimoto, Hitomi Imamura, Atsuhito Ushiki, Shintaro Kanda, Kenji Tsushima, Keishi KuboAbstract:Abstract Human neutrophil elastase (HNE) exists in high concentrations in airway secretions and produces mucus hypersecretion in patients with chronic obstructive pulmonary disease (COPD). l -Carbocisteine improves the quality of life and reduces exacerbation in COPD patients. However the precise mechanism is uncertain. We examined the effects of l -Carbocisteine on HNE-induced mucus hypersecretion and on the production of reactive oxygen species (ROS) which is associated with mucin production induced by HNE. NCI-H292, a human lung mucoepidermoid carcinoma cell line, was treated with or without HNE and l -Carbocisteine. MUC5AC mRNA expression and ROS production in the cells, and MUC5AC protein concentration in supernatants were measured. HNE increased MUC5AC mRNA expression and MUC5AC protein concentration in supernatants in the cells. l -Carbocisteine reduces HNE-induced mRNA expression and protein secretion of MUC5AC. l -Carbocisteine also reduced ROS production in the cells induced by HNE. Reduction of HNE-induced mucus secretion by l -Carbocisteine in the pulmonary epithelial cells may partly relate to the reduction of ROS.
E. Puchelle - One of the best experts on this subject based on the ideXlab platform.
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Carbocisteine improves the mucociliary transport rate in rats with so2 induced bronchitis
Fundamental & Clinical Pharmacology, 1993Co-Authors: J. M. Zahm, J. Levrier, D. Duval, Denis Pierrot, E. PuchelleAbstract:In order to study the effect of Carbocisteine on the mucociliary function of the respiratory tract, we performed a double-blind study on rats with SO 2 -induced (400 ppm) hypersecretion. During the experimental bronchitis, the treated group of rats received Carbocisteine through a stomach tube at a dose level of 500 mg/kg for 15 days, whereas the untreated group of rats received distilled water. After killing the rats, and following lung excision, the respiratory mucus was scraped off and collected by using a glass capillary. The mucus degree of purulence was macroscopically estimated and the mucus transport rate was measured by using the frog palate technique
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Carbocisteine improves the mucociliary transport rate in rats with SO2‐induced bronchitis
Fundamental & clinical pharmacology, 1993Co-Authors: J. M. Zahm, J. Levrier, D. Duval, Denis Pierrot, E. PuchelleAbstract:In order to study the effect of Carbocisteine on the mucociliary function of the respiratory tract, we performed a double-blind study on rats with SO 2 -induced (400 ppm) hypersecretion. During the experimental bronchitis, the treated group of rats received Carbocisteine through a stomach tube at a dose level of 500 mg/kg for 15 days, whereas the untreated group of rats received distilled water. After killing the rats, and following lung excision, the respiratory mucus was scraped off and collected by using a glass capillary. The mucus degree of purulence was macroscopically estimated and the mucus transport rate was measured by using the frog palate technique
J. Levrier - One of the best experts on this subject based on the ideXlab platform.
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Carbocisteine improves the mucociliary transport rate in rats with so2 induced bronchitis
Fundamental & Clinical Pharmacology, 1993Co-Authors: J. M. Zahm, J. Levrier, D. Duval, Denis Pierrot, E. PuchelleAbstract:In order to study the effect of Carbocisteine on the mucociliary function of the respiratory tract, we performed a double-blind study on rats with SO 2 -induced (400 ppm) hypersecretion. During the experimental bronchitis, the treated group of rats received Carbocisteine through a stomach tube at a dose level of 500 mg/kg for 15 days, whereas the untreated group of rats received distilled water. After killing the rats, and following lung excision, the respiratory mucus was scraped off and collected by using a glass capillary. The mucus degree of purulence was macroscopically estimated and the mucus transport rate was measured by using the frog palate technique
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Carbocisteine improves the mucociliary transport rate in rats with SO2‐induced bronchitis
Fundamental & clinical pharmacology, 1993Co-Authors: J. M. Zahm, J. Levrier, D. Duval, Denis Pierrot, E. PuchelleAbstract:In order to study the effect of Carbocisteine on the mucociliary function of the respiratory tract, we performed a double-blind study on rats with SO 2 -induced (400 ppm) hypersecretion. During the experimental bronchitis, the treated group of rats received Carbocisteine through a stomach tube at a dose level of 500 mg/kg for 15 days, whereas the untreated group of rats received distilled water. After killing the rats, and following lung excision, the respiratory mucus was scraped off and collected by using a glass capillary. The mucus degree of purulence was macroscopically estimated and the mucus transport rate was measured by using the frog palate technique
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Study on the effect of oral administration of carbocysteine on ventilatory parameters in the SO2 inhalation model of bronchitis in the rat.
Fundamental & clinical pharmacology, 1992Co-Authors: J. Levrier, D. Duval, K.g. LloydAbstract:Summary— In order to study the physiological correlates of the beneficial action of Carbocisteine (S-carboxy-methyl-cysteine), we have measured the changes occurring in ventilatory parameters in rats made bronchitic by prolonged exposure (2 weeks) to air containing sulfur dioxide (SO2). In animals treated with distilled water (1 ml/100 g/day), statistically significant (P < 0.05) changes in respiratory frequency (-20%) and tidal volume (+ 31%) were found. As a result of these opposing changes, the ventilation/min was stable. Moreover, the compliance was decreased (33%, P < 0.05) and the resistance was greatly enhanced (+ 99%, P < 0.05). The concomitant administration of Carbocisteine (500 mg/kg po/day) with SO2 inhalation significantly (P < 0.05) prevented the development of resistance without effecting significant changes in the other parameters except for a slight improvement in ventilation/min. In conclusion, this improved respiratory resistance in the bronchitic Carbocisteine-treated animals tallies with a decrease in mucus retention associated with the return to normal of rheological characteristics of the secreted mucus.