In vitro and in vivo protection provided by pinocembrin against lipopolysaccharide-induced inflammatory responses
In vitro and in vivo protection provided by pinocembrin against lipopolysaccharide-induced inflammatory responses
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Pinocembrin 对脂多糖诱导的炎症反应提供体外和体内保护
DOI：
10.1016/j.intimp.2012.06.009
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发表时间：
2012-09-01
影响因子：
5.6
通讯作者：
Deng, Xuming
中科院分区：
文献类型：
--
作者：
Soromou, Lanan Wassy;Chu, Xiao;Deng, Xuming
木犀草素或5，7-二羟基黄烷酮是一种黄烷酮，是类黄酮的一种。在本研究中，我们首先评估了松膜蛋白在生巨噬细胞中的抗炎作用，并在此基础上研究了松膜蛋白对内毒素诱导的小鼠急性肺损伤的治疗作用。我们发现，松膜蛋白在体外通过抑制I-kappa Bα、ERK1/2、JNK和p38MAPK的磷酸化而显著调节INF-α、IL-1β、IL-6和IL-10的产生。在脂多糖诱导的小鼠急性肺损伤模型上，腹腔注射松膜素(20或50 mg/kg)。减轻肺水肿的发展，减轻组织学严重度，减轻中性粒细胞、淋巴细胞和巨噬细胞的浸润，并使其增加。此外，松膜素预处理后，IL-10、IL-10、IL-6、IL-1β、INF-α水平显著降低，IL-10水平显著升高。我们的结果还表明，松膜蛋白通过抑制I kappa Bα、JNK和p38MAPK的激活而减轻内毒素诱导的肺损伤。这些发现表明，松膜蛋白可能是调节炎症反应的一种新的候选物质。(C)2012爱思唯尔B.V.保留所有权利。
Pinocembrin or 5, 7-dihydroxyflavanone is a flavanone, a type of flavonoid. In the present study, we first assessed the anti-inflammatory effects of pinocembrin in RAW macrophage cells; and based on these effects, we investigated the therapeutic effects of pinocembrin in murine model of endotoxin-induced acute lung injury. We found that in vitro pretreatment with pinocembrin remarkably regulated the production of INF-alpha, IL-1 beta, IL-6 and IL-10 via inhibiting the phosphorylation of I kappa B alpha, ERK1/2, JNK and p38MAPK. In the mouse model of LPS-induced acute lung injury, pinocembrin (20 or 50 mg/kg, i.p.) attenuated the development of pulmonary edema, histological severities, as well as neutrophil, lymphocyte and macrophage infiltration, which were increased by LPS administration. Additionally, INF-alpha, IL-1 beta and IL-6 concentrations decreased significantly while the concentration of IL-10 was significantly increased after pinocembrin pretreatment. Our results also showed that pinocembrin attenuated LPS-induced lung injury through suppression of I kappa B alpha, JNK and p38MAPK activation. These findings suggest that pinocembrin may represent a novel candidate for the modulation of inflammatory responses. (c) 2012 Elsevier B.V. All rights reserved.