Li Yuexia, Li Xiaohui, Liu Gang, Sun Rongqing, Wang Lirui, Wang Jing, Wang Hongmin
Intensive Care Unit, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.
Department of Cardiovascular Surgery, Henan Provincial People's Hospital, Zhengzhou, Henan Province, China.
J Surg Res. 2015 May 15;195(2):515-21. doi: 10.1016/j.jss.2014.12.054. Epub 2015 Jan 10.
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.
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.
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.
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.
据报道,岩藻甾醇具有抗氧化、抗糖尿病和抗炎作用。在本研究中,我们研究了岩藻甾醇对脂多糖(LPS)诱导的小鼠急性肺损伤(ALI)的保护作用及其可能机制。
通过组织学研究、肺水肿以及支气管肺泡灌洗液中炎性细胞因子的产生来评估肺损伤。在有或没有岩藻甾醇存在的情况下,用LPS刺激肺泡巨噬细胞。通过酶联免疫吸附测定法测定炎性细胞因子的表达。通过蛋白质免疫印迹法检测核因子-κB(NF-κB)的表达。
结果表明,岩藻甾醇减轻了LPS诱导的小鼠ALI中的肺组织病理学变化、湿干比以及肿瘤坏死因子-α、白细胞介素(IL)-6和IL-1β的产生。同时,岩藻甾醇抑制了LPS刺激的肺泡巨噬细胞中NF-κB的激活以及肿瘤坏死因子-α、IL-6和IL-1β的产生。
总之,本研究表明岩藻甾醇对LPS诱导的急性肺损伤具有保护作用,其可能机制是抑制NF-κB激活,从而抑制LPS诱导的炎症反应。