• Liguo Wei, Hiroko Matsumoto, and Hidenori Yamaguchi.
• Department of Anesthesiology, Nihon University School of Dentistry at Matsudo, 2-870-1 Sakaecho-Nishi, Matsudo, Chiba, Japan. wlg5616854@msn.cn
• J Anesth. 2013 Jun 1;27(3):366-73.

PurposePropofol is widely used in sedation and surgical procedures involving patients with acute lung injury (ALI), a common complication in critically ill patients. Monocyte chemoattractant protein-1 (MCP-1) plays an important role in pathological changes in ALI. The present study investigated the anti-inflammatory effect and mechanism of propofol on MCP-1 production and mitogen-activated protein kinase (MAPK) phosphorylation induced by lipopolysaccharide (LPS) in alveolar epithelial cells (AECs).MethodsAECs were treated with 1 μg/ml LPS for 30 min, 1 h, 6 h, or 24 h following pretreatment with 12.5-100 μM propofol for 30 min. Cytokines and chemokines secretion were profiled using cytokine array, and mRNA and protein levels of MCP-1 were measured by RT-PCR and ELISA. The phosphorylation of p38 MAPK, p44/42 MAPK, SAPK/JNK, ATF-2, and c-Jun were measured by Western blot analysis.ResultsPropofol at 50 and 100 μM dose-dependently inhibited MCP-1 mRNA expression (P < 0.05), and also propofol at 50 μM decreased extracellular MCP-1 protein levels (P < 0.05) compared to the LPS group. Propofol at 12.5-50 μM inhibited LPS-induced phosphorylation of p38 MAPK, p44/42 MAPK, SAPK/JNK, ATF-2, and c-Jun in AECs.ConclusionsPropofol at clinically relevant concentrations attenuated LPS-induced MCP-1 mRNA expression and secretion by inhibiting the phosphorylation of p38 MAPK, SAPK/JNK, ATF-2, and c-Jun exerting its anti-inflammatory effects in AECs. These results suggest that propofol may modulate inflammatory response at clinically achievable concentrations in ALI.

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