Antioxidants as Novel Agents for Asthma

Park, Seoung Ju; Lee, Yong Chul

doi:10.2174/138955706775475948

Cited by 16 publications

(15 citation statements)

References 65 publications

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“…There are many previous evidences that oxidative stress is implicated in the pathogenesis of asthma [36]. An accumulating production of ROS is responsible for tissue injury, airway inflammation, and AHR observed in asthma [37].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of airway inflammation and remodeling by sitagliptin in murine chronic asthma

Nader

2015

International Immunopharmacology

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Section: Discussionmentioning

confidence: 99%

Inhibition of airway inflammation and remodeling by sitagliptin in murine chronic asthma

Nader

2015

International Immunopharmacology

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“…Therefore, regulating the ROS levels is critical in the management and amelioration of asthma. It has been suggested that antioxidant(s) or the compounds that could block the ROS-induced inflammatory signals could be excellent drugs for asthma [32–34]. Further, several pharmacological anti-inflammatory agents that inhibit specific signaling kinases such as MAPK (p38, ERK1/2), PI3K, GSK-3β and transcription factors such as NF-κB and AP-1 have been suggested for the amelioration of airway inflammation in asthma [35–40].…”

Section: Discussionmentioning

confidence: 99%

Aldose reductase inhibition suppresses airway inflammation

Yadav

Ramana²,

Srivastava³

2011

Chemico-Biological Interactions

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Airway inflammation induced by reactive oxygen species-mediated activation of redox-sensitive transcription factors is the hallmark of asthma, a prevalent chronic respiratory disease. In various cellular and animal models, we have recently demonstrated that, in response to multiple stimuli, aldose reductase (AKR1B1) regulates the inflammatory signals via NF-kappa B activation. Since NF-κB activation is implicated in asthma pathogenesis, we investigated whether AKR1B1 inhibition could prevent ovalbumin (Ova)- and ragweed pollen extract (RWE)-induced airway inflammation and hyper-responsiveness in mice models and tumor necrosis factor-alpha (TNF-α)-, lipopolysachharide (LPS)- and RWE-induced cytotoxic and inflammatory signals in primary human small airway epithelial cells (SAEC). Sensitization and challenge with Ova or RWE caused airway inflammation and production of inflammatory cytokines, accumulation of eosinophils in airways and sub-epithelial regions, mucin production in the bronchoalveolar lavage fluid, airway hyperresponsiveness, elevated IgE levels and release of Th2 cytokines in the airway and treatment with AKR1B1 inhibitors markedly reduced these pathological changes in mice. In SAEC, treatment with TNF-α, LPS or RWE induced apoptosis, reactive oxygen species generation, synthesis of inflammatory markers IL-6, IL-8, and PGE2 and activation of NF-κB and AP-1. Pharmacological inhibition prevented these changes suggesting that AKR1B1 mediates ROS induced inflammation in small airway epithelial cells. Our results indicate that AKR1B1 inhibitors may offer a novel therapeutic approach to treat inflammatory airway diseases such as asthma.

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“…The extract E. hirta was demonstrated effectively in protecting the liver from toxic hepatitis. Martinez-Vazquez et al, 1999;Pinn, 2001;Mukherjee et al, 2004;Abu-Sayeed et al, 2005;Park & Lee, 2006;Shih et al, 2010 …”

Section: Flavonoidsmentioning

confidence: 99%

“…hirta has been used to treated asthma as a folk medicine (Watanabe et al, 2005). E. hirta functions for the treatment of asthma is probably through synergistic anti-inflammatory and antioxidant activities of especially the flavonoids, sterols and triterpenoids (Park & Lee, 2006). Asthma has long been associated with chronic inflammation and an overall increase in reactive groups and oxidative stress (Nadeem et al, 2003).…”

Section: Inhibition Of Allergic Reactions and Asthma By E Hirtamentioning

confidence: 99%