Therapeutic effects of inhaling aerosolized surfactant alone or with dexamethasone generated by a novel noninvasive apparatus on acute lung injury in rats

Yan, Yongmei; Li, Yidong; Song, Xing-Lei; Liu, Mingyao; Diao, Fei; Wang, Yan; Sun, Yinghao; Wang, Zhihong; Lü, Jing

doi:10.1097/ta.0b013e318265cbe9

Cited by 9 publications

(8 citation statements)

References 27 publications

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“…ARDS is a non-cardiogenic pulmonary edema secondary to alveolar damage after inflammatory process. However, the pathogenesis of this disease remains to be elucidated ( 10 ). It was believed initially that the primary cause of ALI is the cell activation caused by pathogenic factors and body fluid, leading to inflammatory response syndrome and pathological processes, such as alveolar collapse, imbalance of ventilation/perfusion ratio and decreased lung compliance ( 11 ).…”

Section: Discussionmentioning

confidence: 99%

Protective mechanism of sulforaphane in Nrf2 and anti-lung injury in ARDS rabbits

Sun

Niu

et al. 2018

Exp Ther Med

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The effect of sulforaphane on nuclear factor erythroid 2-related factor 2 (Nrf2) and its protective mechanism for lung injury in rabbits with acute respiratory distress syndrome (ARDS) were investigated. Thirty rabbits were randomly divided into control (n=10), model (n=10) and experimental groups (n=10). Rabbits in model group and experimental group were treated with femoral venous injection of oleic acid to establish the ARDS model, while those in control group were injected with the same volume of normal saline. The experimental group received intravenous injection of sulforaphane. Twelve hours after modeling, the clinical manifestations and deaths of rabbits in each group were recorded and compared, including blood gas indexes, lung index (LI), alveolar damage coefficient, serum Nrf2 expression, as well as messenger ribonucleic acid (mRNA) and protein expression of Nrf2 in lung tissues. Pink frothy sputum and death were observed in rabbits in model group and experimental group, but the number of such cases in experimental group was smaller than that in the model group (p<0.05). Compared with those in control group, LI and IQA in model group and experimental group were increased, but LI and IQA in the experimental group were significantly decreased compared with those in the model group. Compared with those in the model group, the blood gas indexes (PaO2, PaCO2 and SaO2) in the experimental group were significantly increased (p<0.05). Nrf2 in serum and lung tissues of rabbits in experimental group was significantly increased compared with that in model group (p<0.05). Sulforaphane significantly inhibits ARDS in rabbits and plays a protective role in ARDS through upregulating Nrf2.

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Section: Discussionmentioning

confidence: 99%

Protective mechanism of sulforaphane in Nrf2 and anti-lung injury in ARDS rabbits

Sun

Niu

et al. 2018

Exp Ther Med

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“…Moreover, the mechanisms responsible for the development of ALI/ARDS are complex and are not yet fully understood (4,5). Currently, clinical therapy is mainly comprehensive, and no specific treatment method is available (6). Consequently, studies on the prevention and treatment of ALI/ARDS are of great importance (4).…”

Section: Introductionmentioning

confidence: 99%

Sulforaphane exerts anti-inflammatory effects against lipopolysaccharide-induced acute lung injury in mice through the Nrf2/ARE pathway

Yan

et al. 2015

International Journal of Molecular Medicine

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Sulforaphane (1-isothiocyanate-4-methyl sulfonyl butane) is a plant extract (obtained from cruciferous vegetables, such as broccoli and cabbage) and is known to exert anticancer, antioxidant and anti-inflammatory effects. It stimulates the generation of human or animal cells, which is beneficial to the body. The aim of the current study was to determine whether sulforaphane protects against lipopolysaccharide (LPS)‑induced acute lung injury (ALI) through its anti-inflammatory effects, and to investigate the signaling pathways involved. For this purpose, male BALB/c mice were treated with sulforaphane (50 mg/kg) and 3 days later, ALI was induced by the administration of LPS (5 mg/kg) and we thus established the model of ALI. Our results revealed that sulforaphane significantly decreased lactate dehydrogenase (LDH) activity (as shown by LDH assay), the wet-to-dry ratio of the lungs and the serum levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) (measured by ELISA), as well as nuclear factor-κB protein expression in mice with LPS-induced ALI. Moreover, treatment with sulforaphane significantly inhibited prostaglandin E2 (PGE2) production, and cyclooxygenase-2 (COX-2), matrix metalloproteinase-9 (MMP-9) protein expression (as shown by western blot analysis), as well as inducible nitric oxide synthase (iNOS) activity in mice with LPS-induced ALI. Lastly, we noted that pre-treatment with sulforaphane activated the nuclear factor-E2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway in the mice with LPS-induced ALI. These findings demonstrate that sulforaphane exerts protective effects against LPS-induced ALI through the Nrf2/ARE pathway. Thus, sulforaphane may be a potential a candidate for use in the treatment of ALI.

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“…IL-1β has a pivotal role in acute lung damage, 28 which is involved in increasing other proinflammatory cytokines such as TNF-α, induction of endothelium damage and apoptosis, enhancing vascular endothelial and alveolar epithelial permeability, contributing to edema, finally leading to cell death and epithelial barrier dysfunction. 29,30 IL-1β can cause ALI through alphavbeta5 and alphavbeta6 integrin-dependent mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Dopamine D1 receptor agonist A-68930 inhibits NLRP3 inflammasome activation and protects rats from spinal cord injury-induced acute lung injury

Jiang

et al. 2016

Spinal Cord

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Therapeutic effects of inhaling aerosolized surfactant alone or with dexamethasone generated by a novel noninvasive apparatus on acute lung injury in rats

Cited by 9 publications

References 27 publications

Protective mechanism of sulforaphane in Nrf2 and anti-lung injury in ARDS rabbits

Protective mechanism of sulforaphane in Nrf2 and anti-lung injury in ARDS rabbits

Sulforaphane exerts anti-inflammatory effects against lipopolysaccharide-induced acute lung injury in mice through the Nrf2/ARE pathway

Dopamine D1 receptor agonist A-68930 inhibits NLRP3 inflammasome activation and protects rats from spinal cord injury-induced acute lung injury

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