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

Wang, Wei; Zheng, Jinping; Zhu, Shaoxuan; Guan, Weijun; Chen, Mao; Zhong, Nanshan

doi:10.1016/j.intimp.2014.12.018

Cited by 28 publications

(26 citation statements)

References 26 publications

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“…Apart from the anti-inflammatory capacity reported previously [10] , carbocisteine could suppress IL-6 and IL-8 release and inhibit IL-6, IL-8, TNF-α, IP-10 and MIP-1β mRNA expression after TNF-α stimulation. Our findings were consistent with a previous report which documented that carbocisteine reduced the levels of IL-1β, IL-6, and IL-8 at 5 days following FluA virus infection and diminished baseline concentrations of these cytokines prior to infection in human airway epithelial cells [27] .…”

Section: Discussioncontrasting

confidence: 49%

“…cDNA synthesis and quantitative PCR were performed using standard procedures as described previously [10] . Primers and probes of tested genes are listed in Table 1.…”

Section: Cell Culturementioning

confidence: 99%

“…Furthermore, carbocisteine was capable of attenuating the synthesis of pro-inflammatory cytokines following rhinovirus or respiratory syncytial virus infection [7,8] . It was speculated that the efficacy of carbocisteine in COPD was more closely associated www.nature.com/aps Wang W et al Acta Pharmacologica Sinica npg with its anti-oxidant and anti-inflammatory effects [9] , which have been scarcely reported previously [10] , than with mucolytic activity.…”

Section: Introductionmentioning

confidence: 99%

“…Exploration of the effects on injured alveolar epithelial cells may provide greater insights into the mechanisms of action of medications (ie, mucolytics) in patients with COPD. We have previously revealed that carbocisteine could inhibit the inflammation induced by hydrogen peroxide in human lung alveolar type II epithelial cells (A549 cells) [10] . However, limited information is available about the effects as well as molecular mechanisms of carbocisteine against TNF-α-induced inflammation.…”

Section: Introductionmentioning

confidence: 99%

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Carbocisteine attenuates TNF-α-induced inflammation in human alveolar epithelial cells in vitro through suppressing NF-κB and ERK1/2 MAPK signaling pathways

et al. 2016

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Aim: We previously proven that carbocisteine, a conventional mucolytic drug, remarkably reduced the rate of acute exacerbations and improved the quality of life in the patients with chronic obstructive pulmonary disease. In this study we investigated the mechanisms underlying the anti-inflammatory effects of carbocisteine in human alveolar epithelial cells in vitro. Methods: Human lung adenocarcinoma cell line A549 was treated with TNF-α (10 ng/mL). Carbocisteine was administered either 24 h prior to or after TNF-α exposure. The cytokine release and expression were measured using ELISA and qRT-PCR. Activation of NF-κB was analyzed with Western blotting, immunofluorescence assay and luciferase reporter gene assay. The expression of ERK1/2 MAPK signaling proteins was assessed with Western blotting. Results: Carbocisteine (10, 100, 1000 µmol/L), administered either before or after TNF-α exposure, dose-dependently suppressed TNF-α-induced inflammation in A549 cells, as evidenced by diminished release of IL-6 and IL-8, and diminished mRNA expression of IL-6, IL-8, TNF-α, MCP-1 and MIP-1β. Furthermore, pretreatment with carbocisteine significantly decreased TNF-α-induced phosphorylation of NF-κB p65 and ERK1/2 MAPK, and inhibited the nuclear translocation of p65 subunit in A549 cells. In an NF-κB luciferase reporter system, pretreatment with carbocisteine dose-dependently inhibited TNF-α-induced transcriptional activity of NF-κB. Conclusion: Carbocisteine effectively suppresses TNF-α-induced inflammation in A549 cells via suppressing NF-κB and ERK1/2 MAPK signaling pathways.

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Section: Discussioncontrasting

confidence: 49%

“…cDNA synthesis and quantitative PCR were performed using standard procedures as described previously [10] . Primers and probes of tested genes are listed in Table 1.…”

Section: Cell Culturementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Carbocisteine attenuates TNF-α-induced inflammation in human alveolar epithelial cells in vitro through suppressing NF-κB and ERK1/2 MAPK signaling pathways

et al. 2016

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“…Numerous studies have consistently shown that the contributors were significantly down regulated after applying hydrogen medicine therapy [10, 14,26,27,41]. Besides, with the deepening biological mechanism of hydrogen research being developed, scientists gradually found that hydrogen therapy can significantly suppress many pathological signal transduction channels such as NF-κβ, MAPK, Lyn-P, and MEK-1 as well as ERK1/2 pathways and ultimately achieve the goal of recovery from many diseases [44,45,[49][50][51][52][53]. In addition, it is worth noting that as H2 is moderate enough, it can selectively react with only hydroxyl radicals (•OH) and peroxynitrite(ONOO-), the main contributors of oxidative stress in vitro and in vivo without disturbing metabolic redox reactions …”

Section: Hypothesismentioning

confidence: 99%

Hydrogen Medicine Therapy: An Effective and Promising Novel Treatment for Multiple Organ Dysfunction Syndrome (MODS) Induced by Influenza and Other Viral Infections Diseases?

Hu¹

2017

SOJMID

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Hydrogen, a non-cytotoxic molecule, is one of nature's most simple elements [1,2]. Recent studies revealed that intraperitoneal injection of hydrogen-rich saline has surprising anti-inflammation, anti-oxidant, anti-apoptosis effects and protected organism against polymicrobial sepsis injury, acute peritonitis injury both by reducing oxidative stress and via decreasing mass proinflammatory responses. It is also well known that the majority of viral -induced tissue damage and discomfort are mainly caused by an inflammatory cytokine storm and oxidative stress rather than by virus itself [3][4][5]. Studies have shown that suppressing the cytokine storm and reducing oxidative stress can significantly alleviate the symptoms of influenza and other severe viral infections diseases [3][4][5][6][7]. However, none of the studies have been focused on the solution as an anti-virus infection therapy yet. Therefore, we hypothesize that hydrogen-rich solution therapy may be a safe, reliable, and effective treatment for Multiple Organ Dysfunction Syndrome (MODS) induced by influenza and other viral infectious diseases.

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PM2.5-induced lung inflammation in mice: Differences of inflammatory response in macrophages and type II alveolar cells

et al. 2017

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

Cited by 28 publications

References 26 publications

Carbocisteine attenuates TNF-α-induced inflammation in human alveolar epithelial cells in vitro through suppressing NF-κB and ERK1/2 MAPK signaling pathways

Carbocisteine attenuates TNF-α-induced inflammation in human alveolar epithelial cells in vitro through suppressing NF-κB and ERK1/2 MAPK signaling pathways

Hydrogen Medicine Therapy: An Effective and Promising Novel Treatment for Multiple Organ Dysfunction Syndrome (MODS) Induced by Influenza and Other Viral Infections Diseases?

PM2.5-induced lung inflammation in mice: Differences of inflammatory response in macrophages and type II alveolar cells

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