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Eur J Pharmacol. 2015 Aug 15;761:174-9. doi: 10.1016/j.ejphar.2015.05.003. Epub 2015 May 11.

Salvianolic acid B attenuates lung inflammation induced by cigarette smoke in mice.

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Departmant of Pharmacy, Liaocheng People's Hospital, Liaocheng 252000, Shandong Province, China. Electronic address:
Departmant of Neuroolgy, Liaocheng People's Hospital, Liaocheng 252000, Shandong Province, China.
Liaocheng University, Liaocheng 252000, Shangdong Province, China.


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.


Cigarette smoke; Lung injury; NF-κB; Nrf-2; Salvianolic acid B

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