Fucosterol attenuates lipopolysaccharide-induced acute lung injury in mice

التفاصيل البيبلوغرافية
العنوان: Fucosterol attenuates lipopolysaccharide-induced acute lung injury in mice
المؤلفون: Lirui Wang, Hongmin Wang, Gang Liu, Jing Wang, Xiaohui Li, Rongqing Sun, Yuexia Li
المصدر: Journal of Surgical Research. 195:515-521
بيانات النشر: Elsevier BV, 2015.
سنة النشر: 2015
مصطلحات موضوعية: Lipopolysaccharides, Male, Pathology, medicine.medical_specialty, Lipopolysaccharide, Acute Lung Injury, Stigmasterol, Pharmacology, Lung injury, Proinflammatory cytokine, Mice, chemistry.chemical_compound, medicine, Animals, Lung, Cells, Cultured, Mice, Inbred BALB C, medicine.diagnostic_test, business.industry, NF-kappa B, Interleukin, respiratory system, Pulmonary edema, medicine.disease, Bronchoalveolar lavage, chemistry, Cytokines, Surgery, Tumor necrosis factor alpha, business, Fucosterol
الوصف: Background Fucosterol has been reported to have antioxidant, antidiabetic, and anti-inflammatory effects. In this study, we investigated the protective effect and the possible mechanism of fucosterol on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Methods Lung injury was assessed by a histologic study, pulmonary edema, and inflammatory cytokines production in bronchoalveolar lavage fluid. Alveolar macrophages were stimulated with LPS in the presence or absence of fucosterol. The expressions of inflammatory cytokines were determined by enzyme-linked immunosorbant assay. Nuclear factor-kappa B (NF-κB) expression was detected by Western blotting. Results The results showed that fucosterol attenuated lung histopathologic changes, wet-to-dry ratio, and tumor necrosis factor-α, interleukin (IL)-6 and IL-1β production in LPS-induced ALI in mice. Meanwhile, fucosterol inhibited NF-κB activation and tumor necrosis factor-α, IL-6, and IL-1β production in LPS-stimulated alveolar macrophages. Conclusions In conclusion, the present study demonstrated that fucosterol exhibited a protective effect on LPS-induced acute lung injury, and the possible mechanism is involved in inhibiting NF-κB activation, thereby inhibiting LPS-induced inflammatory response.
تدمد: 0022-4804
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7dbe068136f216cf4df7fcd17a505ffdTest
https://doi.org/10.1016/j.jss.2014.12.054Test
حقوق: CLOSED
رقم الانضمام: edsair.doi.dedup.....7dbe068136f216cf4df7fcd17a505ffd
قاعدة البيانات: OpenAIRE