Salidroside protects lipopolysaccharide-induced acute lung injury by regulating miR-145/ cytosolic phospholipase A2

Salidroside is one of the main active components from the root of Rhodiola rosea . Previous reports showed that salidroside exhibits anti-inflammatory properties, but the underlying mechanisms are not fully understood. Here, we observed the effects of salidroside on lipopolysaccharide (LPS)-induced acute lung injury (ALI) both in vivo and in vitro . As revealed by survival study, salidroside reduced mortality of rats and prolonged their survival time. Meanwhile, salidroside significantly improved LPS-induced lung histopathologic changes, decreased lung wet-to-dry and lung-to-body weight ratios, inhibited lung myeloperoxidase (MPO) activity. Salidroside also suppressed the expression of cytosolic PLA 2 (cPLA 2 ), the activity of phospholipase A 2 (PLA 2 ) in LPS-treated rats and the metabolites of PLA 2 in bronchoalveolar lavage fluid (BALF), which was confirmed by results of prostaglandin E 2 (PGE 2 ), leukotriene B 4 (LTB 4 ) and thromboxane B 2 (TXB 2 ) detection. And the expression of microRNA-145 in LPS-treated rats was up-regulated by salidroside. Besides, salidroside raised the level of miR-145and reduced PLA 2 activity in LPS-induced A549 cells in a concentration-dependent manner, which was obviously reversed by miR-145 inhibition. In conclusion, the current study demonstrated that salidroside exhibited a protective effect on LPS-induced ALI by inhibiting of the inflammatory response, which may involve in the up-regulation of miR-145 and the suppression of cPLA 2 . Highlights Salidroside reduces acute lung injury by inhibiting the increment and metabolism of phospholipase A2; Salidroside inhibits LPS-induced PLA2 increase dependent on miR-145; The inhibitory effect of Salidroside on Phospholipases A2 provides a link between the identification of new targets and potential new therapeutic agents for the treatment of acute lung injury.