Diethylcarbamazine inhibits NF-κB activation in acute lung injury induced by carrageenan in mice

Santos, Laise Aline Martins dos; Ribeiro, Edlene Lima; Barbosa, Karla Patrícia Sousa; Fragoso, Ingrid Tavares; Gomes, Fabiana Oliveira dos Santos; Donato, Mariana Aragão Matos; Silva, Bruna Santos; Silva, Amanda Karolina Soares; Rocha, Sura Wanessa Santos; França, Maria Eduarda Rocha de; Rodrigues, Gabriel Barros; Silva, Teresinha Gonçalves; Peixoto, Christina Alves

doi:10.1016/j.intimp.2014.08.017

Cited by 15 publications

(10 citation statements)

References 37 publications

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“…Its high expression is induced by a variety of genes (26). The activation of NF-κB induces the activation of COX-2, which may increase the levels of the endogenous immune inhibitor, PGE2, which causes immunosuppression following infection, thus increasing the occurrence rate of lung injury and the fatality rate (27). In the present study, sulforaphane significantly suppressed NF-κB and COX-2 protein expression in mice with LPS-induced ALI.…”

Section: Discussionsupporting

confidence: 50%

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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Section: Discussionsupporting

confidence: 50%

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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“…However, other doses could show also inhibitive effect. This finding was also observed in previous studies on DEC antiinflammatory action [10,11]. This confirms the inhibitive action of DEC on intracellular signaling pathways which interfere with insulin-receptor signaling.…”

Section: Discussionsupporting

confidence: 90%

“…This dose was also the most effective for reduction of inflammatory markers released from inflammed adipose tissue. The same dose was formerly found to depress the induced inflammatory responses in liver and lung [10,13]. Thus, the anti-inflammatory action of DEC was limited to the application of 50 mg/kg.…”

Section: Discussionmentioning

confidence: 99%

“…It inhibits prostaglandins for the clearance of blood microfilariae [9]. DEC has been known as an anti-inflammatory drug because of its success to reduce the experimentally induced inflammation in lung and liver [10,11]. These reduced inflammatory responses could be attributed to the inactivation of NF-κB and thus suppressing the induction of NF-κB-dependent genes.…”

Section: Introductionmentioning

confidence: 99%

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Diethylcarbamazine citrate ameliorates insulin resistance in high-fat diet-induced obese mice via modulation of adipose tissue inflammation

Abdel‐Latif

2015

International Immunopharmacology

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“…Samples were collected 4 h after the induction of pleurisy, with PBS and 10 mM indomethacin, and then were centrifuged at 1200 g for 10 min at 4 C, followed by separation and storage (À70 C) of the supernatant until the assay. Then, the basal PGE 2 values were removed from all of the samples [40].…”

Section: Measurement Of Prostaglandin E 2 (Pge 2 )mentioning

confidence: 99%

Potential anti-inflammatory effect of LQFM-021 in carrageenan-induced inflammation: The role of nitric oxide

Florentino

Silva

et al. 2017

Nitric Oxide

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The pyrazole compound LQFM-021 exhibits vasorelaxant, antinociceptive and anti-inflammatory activities. Furthermore, it has low toxicity, indicating that this compound may be considered to be a good prototype for the development of new analgesic/anti-inflammatory drugs. Therefore, the aim of this study was to investigate the potential anti-inflammatory activity of LQFM-021 using a model of carrageenan-induced inflammation as well as the mechanism of action and role of nitric oxide in this effect. Acute treatments with LQFM-021 (30 and 60 mg/kg p.o.) reduced paw edema formation dose-dependently 2 h after carrageenan injection. In the carrageenan-induced pleurisy test, LQFM-021 (30 mg/kg p.o.) reduced the leukocyte (polymorphonuclear) count in the pleural cavity, as well as decreased protein extravasation and myeloperoxidase activity. This dose of LQFM-021 increased the NO (nitrite/nitrate) and IL-4 levels and decreased the TNF-α and IL-1β levels in the pleural cavity. Moreover, pre-treatment with L-NAME reversed the effect of LQFM-021 on NO, leukocyte migration, and the TNF-α and IL-1β levels. Additionally, we observed that LQFM-021 showed weak inhibitory activity on cyclooxygenases, but reduced the PGE levels in the pleural cavity. Immunoblot analyses showed that LQFM-021 promoted a decrease in COX-2 levels and increase in iNOS levels. In conclusion, we demonstrated that LQFM-021 has marked anti-inflammatory activity by reducing polymorphonuclear recruitment, which is associated with the inhibition of the production of inflammatory cytokines and eicosanoids. In addition, we found that the synthase/release of nitric oxide promoted by LQFM-021 is essential for the anti-inflammatory effect observed.

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Diethylcarbamazine inhibits NF-κB activation in acute lung injury induced by carrageenan in mice

Cited by 15 publications

References 37 publications

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

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

Diethylcarbamazine citrate ameliorates insulin resistance in high-fat diet-induced obese mice via modulation of adipose tissue inflammation

Potential anti-inflammatory effect of LQFM-021 in carrageenan-induced inflammation: The role of nitric oxide

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