Jin-Long Yu1, Xiao-Shi Zhang2, Xia Xue1, Rong-Mei Wang3. 1. Department of Pharmacy, The Second Hospital of Shandong University, Jinan, Shandong, China. 2. Department of Clinical Laboratory, Qilu Hospital, Shandong University, Jinan, Shandong, China. 3. Department of Pharmacy, The Second Hospital of Shandong University, Jinan, Shandong, China. Electronic address: wangrongmeiyl@163.com.
Abstract
BACKGROUND: Patchouli alcohol (PA), a natural compound isolated from Pogostemon cablin, has been reported to possess anti-inflammatory activity. However, the effects of PA on lipopolysaccharide (LPS)-induced acute lung injury (ALI) have not yet been studied. In the present study, we investigated in vivo the effect of PA on ALI induced by LPS. METHODS: Mice were administrated intranasally with LPS to induce lung injury. PA was administrated intraperitoneally 1 h before or after the LPS challenge. RESULTS: The results showed that PA significantly decreased the wet-to-dry weight ratio of lungs and the number of total cells, neutrophils, and macrophages in bronchoalveolar lavage fluid at 7 h after the LPS challenge. In addition, PA also suppressed the production of inflammatory cytokines, such as tumor necrosis factor-α, interleukin-1β, and interleukin-6 in bronchoalveolar lavage fluid. Furthermore, Western blot analysis showed that PA inhibited the phosphorylation of IκB-α and p65 nuclear factor κB (NF-κB) induced by LPS. CONCLUSIONS: Our results suggest that the anti-inflammatory effects of PA against LPS-induced ALI may be due to its ability to inhibit NF-κB signaling pathways.
BACKGROUND:Patchouli alcohol (PA), a natural compound isolated from Pogostemon cablin, has been reported to possess anti-inflammatory activity. However, the effects of PA on lipopolysaccharide (LPS)-induced acute lung injury (ALI) have not yet been studied. In the present study, we investigated in vivo the effect of PA on ALI induced by LPS. METHODS:Mice were administrated intranasally with LPS to induce lung injury. PA was administrated intraperitoneally 1 h before or after the LPS challenge. RESULTS: The results showed that PA significantly decreased the wet-to-dry weight ratio of lungs and the number of total cells, neutrophils, and macrophages in bronchoalveolar lavage fluid at 7 h after the LPS challenge. In addition, PA also suppressed the production of inflammatory cytokines, such as tumor necrosis factor-α, interleukin-1β, and interleukin-6 in bronchoalveolar lavage fluid. Furthermore, Western blot analysis showed that PA inhibited the phosphorylation of IκB-α and p65 nuclear factor κB (NF-κB) induced by LPS. CONCLUSIONS: Our results suggest that the anti-inflammatory effects of PA against LPS-induced ALI may be due to its ability to inhibit NF-κB signaling pathways.