Zhang Dong-Fang, Zhang Jin, Li Ran
Departmant of Pharmacy, Liaocheng People's Hospital, Liaocheng 252000, Shandong Province, China.
Departmant of Neuroolgy, Liaocheng People's Hospital, Liaocheng 252000, Shandong Province, China.
Eur J Pharmacol. 2015 Aug 15;761:174-9. doi: 10.1016/j.ejphar.2015.05.003. Epub 2015 May 11.
Salvianolic acid B (Sal B), a bioactive compound isolated from the Chinese herb Radix Salviae Miltiorrhizae, has been reported to exhibit anti-inflammatory and anti-oxidantive effects. The aim of this study was to investigate the protective effects of Sal B on cigarette smoke (CS)-induced acute lung inflammation. Sal B was given intraperitoneally (i.p.) to mice 1h before CS exposure daily for four consecutive days. Bronchoalveolar lavage fluid (BALF) was collected to assess the levels of inflammatory cytokines and cell counts. Lung tissues were used to analysis pathological changes, total glutathione (GSH), nuclear factor erythroid-2 related factor 2 (Nrf-2), and nuclear factor-kappa B (NF-κB) expression. The results showed that Sal B inhibited CS-induced lung pathological changes, the infiltration of inflammatory cells, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), and monocyte chemoattractant protein 1 (MCP-1) productions. Sal B also up-regulated CS-induced total glutathione (GSH) production. Furthermore, Sal B was found to up-regulate Nrf-2, hemeoxygenase1 (HO1) expression and suppress CS-induced NF-κB activation. In conclusion, the current study demonstrated that Sal B exhibited a protective effect on CS-induced lung injury and the possible mechanism was involved in activating Nrf-2 and inhibiting NF-κB activation.
丹酚酸B(Sal B)是从中药丹参中分离出的一种生物活性化合物,据报道具有抗炎和抗氧化作用。本研究旨在探讨Sal B对香烟烟雾(CS)诱导的急性肺部炎症的保护作用。在连续四天每天CS暴露前1小时,给小鼠腹腔注射(i.p.)Sal B。收集支气管肺泡灌洗液(BALF)以评估炎症细胞因子水平和细胞计数。用肺组织分析病理变化、总谷胱甘肽(GSH)、核因子红细胞2相关因子2(Nrf-2)和核因子κB(NF-κB)表达。结果表明,Sal B抑制了CS诱导的肺部病理变化、炎症细胞浸润、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)和单核细胞趋化蛋白1(MCP-1)的产生。Sal B还上调了CS诱导的总谷胱甘肽(GSH)产生。此外,发现Sal B上调Nrf-2、血红素加氧酶1(HO1)表达并抑制CS诱导的NF-κB活化。总之,本研究表明Sal B对CS诱导的肺损伤具有保护作用,其可能机制涉及激活Nrf-2和抑制NF-κB活化。