2013
DOI: 10.1016/j.jep.2013.05.020
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Total flavonoids of Mosla scabra leaves attenuates lipopolysaccharide-induced acute lung injury via down-regulation of inflammatory signaling in mice

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Cited by 27 publications
(17 citation statements)
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“…Regarding the mechanism of action, this flavonoid reduced LPS-induced activation of the MAPK and NFκB pathways [99]. Other works have also studied flavonoids for their beneficial effects in LPS-induced ARDS [97].…”
Section: Acute Respiratory Distress Syndrome (Ards)mentioning
confidence: 99%
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“…Regarding the mechanism of action, this flavonoid reduced LPS-induced activation of the MAPK and NFκB pathways [99]. Other works have also studied flavonoids for their beneficial effects in LPS-induced ARDS [97].…”
Section: Acute Respiratory Distress Syndrome (Ards)mentioning
confidence: 99%
“…Although the control of lung ventilation as a protection strategy has considerably reduced mortality, no specific treatment is available; the number of young people who died because of ARDS is high and the treatment only considered the cause. Some evidence suggests that substances of the flavonoid class may have a modulatory effect in ARDS, but most of the studies are in experimental models [97,98].…”
Section: Acute Respiratory Distress Syndrome (Ards)mentioning
confidence: 99%
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“…It reported that total flavonoids of Mosla scabra (MF) leaves could attenuate pulmonary inflammation in mice with LPS-induced ALI, and the protective effect of MF in ALI might be related to its suppression of NF- κ B and MAPK activation and, subsequently, caused a remarkable reduction in inflammatory cell infiltration and inflammatory cytokine secretion in lung tissues [39]. Also, luteolin suppresses inflammatory mediator expression by blocking the Akt/NF κ B pathway in acute lung injury induced by lipopolysaccharide [40].…”
Section: Discussionmentioning
confidence: 99%
“…It is characterized by neutrophil influx, alveolar-capillary barrier damage leading to interstitial edema, and the impairment of respiratory function [3,4]. While great advances in understanding the pathophysiology of ALI have been reported to date, no effective medicine is available for ALI, and it remains the leading cause of morbidity and mortality in critically ill patients [5,6].…”
Section: Introductionmentioning
confidence: 99%