Shen Yongbin, Sun Zhanfeng, Guo Xiaotong
Department of Vascular Surgery, the 2nd Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Department of Thoracic Surgery, the 2nd Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Eur J Pharmacol. 2015 Jan 15;747:45-51. doi: 10.1016/j.ejphar.2014.09.040. Epub 2014 Oct 2.
Citral, a component of lemongrass oil, has been reported to have many pharmacological activities such as anti-bacterial and anti-inflammatory effects. However, the effects of citral on acute lung injury (ALI) and the molecular mechanisms have not been reported. The aim of this study was to detect the effects of citral on lipopolysaccharide (LPS)-induced acute lung injury and investigate the molecular mechanisms. LPS-induced acute lung injury model was used to detect the anti-inflammatory effect of citral in vivo. The alveolar macrophages were used to investigate the molecular mechanism of citral in vitro. The results showed that pretreatment with citral remarkably attenuated pulmonary edema, histological severities, TNF-α, IL-6 and IL-1β production in LPS-induced ALI in vivo. In vitro, citral inhibited LPS-induced TNF-α, IL-6 and IL-1β production in alveolar macrophages. LPS-induced NF-κB activation was also inhibited by citral. Furthermore, we found that citral activated PPAR-γ and the anti-inflammatory effects of citral can be reversed by PPAR-γ antagonist GW9662. In conclusion, this is the first to demonstrate that citral protects LPS-induced ALI in mice. The anti-inflammatory mechanism of citral is associated with activating PPAR-γ, thereby inhibiting LPS-induced inflammatory response.
柠檬醛是柠檬草油的一种成分,据报道具有多种药理活性,如抗菌和抗炎作用。然而,柠檬醛对急性肺损伤(ALI)的影响及其分子机制尚未见报道。本研究旨在检测柠檬醛对脂多糖(LPS)诱导的急性肺损伤的影响,并探讨其分子机制。采用LPS诱导的急性肺损伤模型检测柠檬醛在体内的抗炎作用。利用肺泡巨噬细胞研究柠檬醛在体外的分子机制。结果表明,柠檬醛预处理可显著减轻LPS诱导的ALI小鼠的肺水肿、组织学严重程度、TNF-α、IL-6和IL-1β的产生。在体外,柠檬醛抑制LPS诱导的肺泡巨噬细胞中TNF-α、IL-6和IL-1β的产生。柠檬醛还抑制LPS诱导的NF-κB活化。此外,我们发现柠檬醛激活PPAR-γ,且柠檬醛的抗炎作用可被PPAR-γ拮抗剂GW9662逆转。总之,这是首次证明柠檬醛可保护LPS诱导的小鼠ALI。柠檬醛的抗炎机制与激活PPAR-γ有关,从而抑制LPS诱导的炎症反应。