Moracin M inhibits airway inflammation by interrupting the JNK/c-Jun and NF-κB pathways in vitro and in vivo

Lee, Ju Hee; Ko, Hae Ju; Woo, Eun‐Rhan; Lee, Sang Kook; Moon, Bong Soo; Lee, Chan Woo; Mandava, Suresh; Samala, Mallesham; Lee, Jong-Kook; Kim, Hyun Pyo

doi:10.1016/j.ejphar.2016.04.055

Cited by 33 publications

(21 citation statements)

References 19 publications

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“…Recently, moracin M (arylbenzofuran, 36) was found to inhibit LPS-induced ALI at 20–60 mg/kg (Lee et al ., 2016). Moracin M was found to suppress NF-κB activation in the inflamed lung.…”

Section: The Inhibition Of Plant Constituents Against In Vivo Animal mentioning

confidence: 99%

Therapeutic Potential of Medicinal Plants and Their Constituents on Lung Inflammatory Disorders

Kim

Lim

Kwon

2016

Biomol Ther (Seoul)

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Acute bronchitis and chronic obstructive pulmonary diseases (COPD) are essentially lung inflammatory disorders. Various plant extracts and their constituents showed therapeutic effects on several animal models of lung inflammation. These include coumarins, flavonoids, phenolics, iridoids, monoterpenes, diterpenes and triterpenoids. Some of them exerted inhibitory action mainly by inhibiting the mitogen-activated protein kinase pathway and nuclear transcription factor-κB activation. Especially, many flavonoid derivatives distinctly showed effectiveness on lung inflammation. In this review, the experimental data for plant extracts and their constituents showing therapeutic effectiveness on animal models of lung inflammation are summarized.

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“…Recently, moracin M (arylbenzofuran, 36) was found to inhibit LPS-induced ALI at 20–60 mg/kg (Lee et al ., 2016). Moracin M was found to suppress NF-κB activation in the inflamed lung.…”

Section: The Inhibition Of Plant Constituents Against In Vivo Animal mentioning

confidence: 99%

Therapeutic Potential of Medicinal Plants and Their Constituents on Lung Inflammatory Disorders

Kim

Lim

Kwon

2016

Biomol Ther (Seoul)

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“…The down‐regulation mechanisms include interruption of the JNK/IKK/NF‐κB pathways, among several signaling pathways leading to iNOS induction (Figure ; Chan & Riches, ). This finding is particularly important because NF‐κB and MAPK activation are important to provoke inflammatory responses in the lung tissue of ALI mice (Chen et al, ; Lee et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…2.5 | Cellular mechanism study of aurantio-obtusin on iNOS-mediated NO production Previously, the appropriate incubation times for enhanced activation of mitogen-activated protein kinases (MAPKs) and signal transcription factors were found as 15 min and 1 hr, respectively (Lee et al, 2016). At this time point, the cell homogenates were prepared for examination of MAPK activation, and the protein levels of signaling molecules were examined by western blotting technique according to the previously described (Lee et al, 2016). of protease inhibitor cocktail) and centrifuged at 13,000 rpm for 10 min.…”

Section: Mh-s Cell Culture and No Productionmentioning

confidence: 99%

“…The inhibitory cellular mechanisms of aurantio-obtusin on iNOS expression were then studied. MAPK pathways are known to be important in the induction of iNOS (Chen et al, 2012;Lee et al, 2016). Therefore, the effect of aurantio-obtusin on MAPK activation 3.4 | Effects of aurantio-obtusin against IL-6 production in IL-1β-treated A549 cells…”

Section: Cellular Action Mechanisms Of Aurantio-obtusin On Inos Dowmentioning

confidence: 99%

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Aurantio‐obtusin, an anthraquinone from cassiae semen, ameliorates lung inflammatory responses

Park

Lim

et al. 2018

Phytotherapy Research

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The purpose of the present study is to find the natural compound(s) having a therapeutic potential to treat lung inflammatory disorders. In our screening procedure, the methanol extract of the seeds of Cassia obtusifolia (cassiae semen) inhibited inducible nitric oxide synthase-catalyzed nitric oxide production in alveolar macrophages (MH-S). From the extract, 8 major anthraquinone derivatives were successfully isolated. They are chrysophanol, physcion, 2-hydroxy-emodin 1-methyl ether, obtusifolin, obtusin, aurantio-obtusin, chryso-obtusin, and gluco-obtusifolin, among which aurantio-obtusin (IC = 71.7 μM) showed significant inhibitory action on nitric oxide production from lipopolysaccharide-treated MH-S cells, mainly by downregulation of inducible nitric oxide synthase expression. This down-regulatory action of aurantio-obtusin was mediated at least in part via interrupting c-Jun N-terminal kinase/IκB kinase/nuclear transcription factor-κB pathways. Aurantio-obtusin also inhibited IL-6 production in IL-1β-treated lung epithelial cells, A549. Importantly, this compound (10 and 100 mg/kg) by oral administration attenuated lung inflammatory responses in a mouse model of lipopolysaccharide-induced acute lung injury. Therefore, it is for the first time found that aurantio-obtusin may have a therapeutic potential for treating lung inflammatory diseases.

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“…ARDS is regarded as part of a systemic inflammatory response, particularly systemic sepsis (24), which is usually accompanied by excessive inflammatory cell infiltration, cascade release of inflammatory factors, and extravasation of protein-rich fluid (25). Previous studies have determined that MAPK signaling pathways may have an important pathogenic role in the inflammatory process associated with sepsis-induced ARDS (19,26,27). As the current study demonstrated, ARDS triggered by sepsis after CLP challenge may induce phosphorylation of JNK and p38 MAPK in the lung tissue and modulation of MAPK signaling by JNK or/and p38 MAPK-specific inhibitor may significantly improve the pulmonary histopathology and lung permeability, increasing the serum levels of anti-inflammatory factors and reducing the serum levels of pro-inflammatory factors in sepsis-induced acute lung injury rats.…”

Section: Discussionmentioning

confidence: 99%

Modulation of mitogen-activated protein kinase attenuates sepsis-induced acute lung injury in acute respiratory distress syndrome rats

Fang

Cai

Wang

et al. 2017

Molecular Medicine Reports

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Sepsis is the most important predisposing cause inducing acute respiratory distress syndrome (ARDS); however, the mechanism of sepsis leading to the development of ARDS remains to be elucidated. Suppression of the mitogen‑activated protein kinase (MAPK) signal by blocking the phosphorylation of Jun N‑terminal kinase (JNK) and p38 in lung tissues could alleviate acute lung injury induced by sepsis. MAPK signaling may have a crucial role in development of the sepsis‑induced acute lung injury. The specific inhibitors of JNK and p38 MAPK, SP600125 and SB203580, were administrated by intragastric injection 4 h before induction of ARDS after cecal ligation and puncture (CLP). Rats were sacrificed at 1, 6 or 24 h after CLP challenge. The histological evaluation, lung water content, and biochemical analysis were performed. The results revealed that the JNK and p38 MAPK inhibitor improved lung permeability, attenuated system inflammation, further alleviated the lung injury induced by sepsis. In conclusion, JNK and p38 MAPK signaling are essential for the development of ARDS following sepsis. Further studies are needed to illuminate the detailed mechanisms of JNK and p38 MAPK signaling in sepsis‑induced ARDS.

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Moracin M inhibits airway inflammation by interrupting the JNK/c-Jun and NF-κB pathways in vitro and in vivo

Cited by 33 publications

References 19 publications

Therapeutic Potential of Medicinal Plants and Their Constituents on Lung Inflammatory Disorders

Therapeutic Potential of Medicinal Plants and Their Constituents on Lung Inflammatory Disorders

Aurantio‐obtusin, an anthraquinone from cassiae semen, ameliorates lung inflammatory responses

Modulation of mitogen-activated protein kinase attenuates sepsis-induced acute lung injury in acute respiratory distress syndrome rats

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