Journal
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
Volume 42, Issue 1, Pages 34-43Publisher
KARGER
DOI: 10.1159/000477112
Keywords
Salidroside; Ventilation; induced lung injury; NLRP3 inflammasome; SIRT1; Cyclic stretch
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Funding
- National Natural Science Foundation of China [81571929, 81272144, 31671213, 31271270, 81372100, 81672266, 31371164]
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Background: Salidroside (SDS) is the main effective ingredient of Rhodiola rosea L with a variety of pharmacologic properties. We aim to investigate the effects of SDS on ventilation induced lung injury (VILI) and explore the possible underlying molecular mechanism. Methods: Lung injury was induced in male ICR mice via mechanical ventilation (30 ml/ kg) for 4h. The mice were divided in four groups:(1) Control group; (2) Ventilation group; (3) SDS group; (4) Ventilation with SDS group. SDS (50 mg/ kg) was injected intraperitoneally 1h before operation. Mouse lung vascular endothelial cells (MLVECs) were subjected to cyclic stretch for 4h. Results: It was found that SDS attenuated VILI as shown in HE staining, cell count and protein content levels in BAL fluid, W/ D and Evans blue dye leakage into the lung tissue. SDS treatment inhibited the activation of NLRP3 inflammasome and subsequent caspase- 1 cleavage as well as interleukin (IL)- 1 beta secretion both in vivo and in vitro. Moreover, SDS administration up- regulated SIRT1 expression. Importantly, knockdown of SIRT1 reversed the inhibitory effect of SDS on NLRP3 inflammasome activation. Conclusions: Taken together, these findings indicate that SDS may confer protection against ventilation induced lung injury via SIRT1- dependent inhibition of NLRP3 inflammasome activation. (C)2017 The Author(s) Published by S. Karger AG, Basel
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