Department of Outpatient Clinic, the Affiliated Hospital of Inner Mongolia University for the Nationalities, Tongliao, 028000, People's Republic of China.
Inflammation. 2013 Apr;36(2):501-11. doi: 10.1007/s10753-012-9571-1.
The present study aimed to investigate the protective role of limonene in lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI was induced in mice by intratracheal instillation of LPS (0.5 mg/kg), and limonene (25, 50, and 75 mg/kg) was injected intraperitoneally 1 h prior to LPS administration. After 12 h, bronchoalveolar lavage fluid (BALF) and lung tissue were collected. Limonene pretreatment at doses of 25, 50, and 75 mg/kg decreased LPS-induced evident lung histopathological changes, lung wet-to-dry weight ratio, and lung myeloperoxidase activity. In addition, pretreatment with limonene inhibited inflammatory cells and proinflammatory cytokines including tumor necrosis factor-α, interleukin-1β, and interleukin-6 in BALF. Furthermore, we demonstrated that limonene blocked the phosphorylation of IκBα, nuclear factor-κB (NF-κB) p65, p38 mitogen-activated protein kinase (MAPK), c-Jun NH2-terminal kinase, and extracellular signal-regulated kinase in LPS-induced ALI. The results presented here suggest that the protective mechanism of limonene may be attributed partly to decreased production of proinflammatory cytokines through the inhibition of NF-κB and MAPK activation.
本研究旨在探讨柠檬烯在脂多糖（LPS）诱导的急性肺损伤（ALI）中的保护作用。通过气管内滴注 LPS（0.5mg/kg）诱导小鼠 ALI，柠檬烯（25、50 和 75mg/kg）在 LPS 给药前 1 小时腹腔内注射。12 小时后，收集支气管肺泡灌洗液（BALF）和肺组织。25、50 和 75mg/kg 的柠檬烯预处理可降低 LPS 诱导的明显肺组织病理学变化、肺湿重/干重比和肺髓过氧化物酶活性。此外，柠檬烯预处理可抑制 BALF 中的炎性细胞和促炎细胞因子，包括肿瘤坏死因子-α、白细胞介素-1β 和白细胞介素-6。此外，我们表明，柠檬烯通过抑制 NF-κB 和 MAPK 激活来阻断 LPS 诱导的 ALI 中 IκBα、核因子-κB（NF-κB）p65、p38 丝裂原活化蛋白激酶（MAPK）、c-Jun NH2-末端激酶和细胞外信号调节激酶的磷酸化。本研究结果表明，柠檬烯的保护机制可能部分归因于通过抑制 NF-κB 和 MAPK 激活减少促炎细胞因子的产生。
