Salidroside attenuates inflammatory response via suppressing JAK2-STAT3 pathway activation and preventing STAT3 transfer into nucleus

• Published in: International immunopharmacology Vol. 35; pp. 265 - 271
• Main Authors: Qi, Zhilin, Qi, Shimei, Ling, Liefeng, Lv, Jun, Feng, Zunyong
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.06.2016
• Subjects: Active Transport, Cell Nucleus - drug effects; Acute lung injury; Acute Lung Injury - drug therapy; Animals; Cell Nucleus - metabolism; Cytokines - metabolism; Glucosides - therapeutic use; Immunosuppressive Agents - therapeutic use; Inflammation; Inflammation - drug therapy; Inflammation - metabolism; Inflammation Mediators - metabolism; JAK2-STAT3; Janus Kinase 2 - metabolism; Lipopolysaccharides - immunology; LPS; Macrophages, Peritoneal - drug effects; Macrophages, Peritoneal - immunology; Mice; Mice, Inbred BALB C; Nitric Oxide Synthase Type II; Phenols - therapeutic use; RAW 264.7 Cells; Salidroside; Signal Transduction - drug effects; STAT3 Transcription Factor - metabolism; Salidroside; Acute lung injury; Inflammation; JAK2-STAT3; LPS

Salidroside (SAL) is an active ingredient isolated from the Rhodiola rosea, has potent anti-inflammatory effect, but the mechanism is still elusive. The purpose of this study is to verify the effects of SAL on LPS-induced inflammatory response and investigate the possible underlying molecular mechan...