Salidroside attenuates inflammatory response via suppressing JAK2-STAT3 pathway activation and preventing STAT3 transfer into nucleus |
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| Institution: | 1. Department of Biochemistry, Wannan Medical College, Wuhu, Anhui, China;2. Anhui Province Key Laboratory of Active Biological Macro-molecules, Wuhu, Anhui, China;1. Clinical Medical College, Chengdu University of TCM, Chengdu 610075, China;2. Department of Ophthalmology, Chengdu University of TCM, Chengdu 610075, China;3. General Clinical Research Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, China;4. Department of Pharmacy, First Affiliated Hospital of Nanjing Medical University, Nanjing, China;5. Department of Traditional Chinese Medicine, The Third People''s Hospital of Chengdu, 82 Qing Long Street, Chengdu 610031, China;6. Neurobiology Laboratory, Jiangsu Center for Drug Screening, China Pharmaceutical University, Jiangsu, Nanjing 210009, China;7. University College London, United Kingdom;1. Cardiovascular Research Center and Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, United States\n;2. Federal State Budgetary Scientific Institution “E.D. Goldberg Institute of Pharmacology and Regenerative Medicine”, 3 Lenin Street, Tomsk 634028, Russia;3. Siberian State Medical University, 2 Moscowsky Trakt 634050, Tomsk, Russia;4. Institute for Problems of Chemical and Energetic Technologies, Siberian Branch of the Russian Academy of Sciences, 1 Socialisticheskaya Street, Biysk, Russia;5. Federal State Budgetary Scientific Institution “Research Institute for Cardiology”, 111a Kievskaya Street, Tomsk 634012, Russia;6. RASA Center in Tomsk, Tomsk Polytechnic University, 30 Lenin Street, Tomsk 634050, Russia |
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| Abstract: | 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 mechanism. RAW264.7 cells were pre-incubated with SAL for 2 h, then stimulated with or without LPS for another 16 h. The levels of TNF-α, MCP-1, IL-6, and PGE2 were detected by ELISA, and the production of NO was determined by nitrite analysis. The expression levels of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were detected by Western blotting. In RAW264.7 cells and murine peritoneal macrophages, the activation of signal molecules was also measured by Western blot. The nuclear translocation of STAT3 was determined by Laser confocal and nucleocytoplasmic separation experiments. Our results showed that SAL attenuated the productions of TNF-α, IL-6, MCP-1, PGE2 and NO dose dependently. SAL also suppressed LPS-induced expressions of iNOS and COX-2 significantly. Further studies revealed that SAL down-regulated the phosphorylation of JAK2-STAT3 signaling pathway and reduced the nuclear translocation of STAT3 induced by LPS in RAW264.7 cells and primary peritoneal macrophages. In addition, consistent with the results in vitro, in the model of mice acute lung injury (ALI) induced by LPS, SAL reduced the infiltration of inflammatory cells and decreased the levels of serum TNF-α and IL-6 obviously. Taken together, these data indicated that SAL exerted anti-inflammatory action via down-regulating LPS-induced activation of JAK2-STAT3 pathway and suppressing STAT3 transfer into the nucleus at least in part. |
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