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ORIGINAL ARTICLE
Year : 2017  |  Volume : 13  |  Issue : 51  |  Page : 378-384

Prim-O-glucosylcimifugin attenuates lipopolysaccharide- induced inflammatory response in RAW 264.7 macrophages


1 Department of Dermatology, Seventh People's Hospital of Shanghai University of TCM, Shanghai 200137, China
2 Department of Clinical Medicine, Bengbu Medical College, Anhui 233000, China
3 Department of Pharmaceutical Botany, School of Pharmacy, Second Military Medical University, Shanghai 200433, China
4 Xinchang Community Health Service Center, Pudong New Area, Shanghai 201314, China
5 Department of Pharmaceutical Botany, School of Pharmacy, Second Military Medical University, Shanghai 200433; Central Laboratory, Seventh People's Hospital of Shanghai University of TCM, Shanghai 200137, China

Correspondence Address:
Hong Zhang
Central Laboratory, Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, 358 Datong Road, Shanghai 200137
China
Wei-An Mao
Xinchang Community Health Service Center, Pudong New Area, 58 West Pailou Road, Shanghai 201314
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pm.pm_323_16

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Background: Radix Saposhnikoviae (RS) exerts anti-inflammatory, analgesic, antipyretic, antioxidation effects and has been used in traditional Chinese medicine to treat common colds, headache, and rheumatoid arthritis. Prim-O-glucosylcimifugin (POG) is the highest content chromone and one of the major active constituents in RS. Objective: The study was aimed to explore the anti-inflammation effects of POG in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Materials and Methods: Cell viability was detected by Cell Counting Kit-8 assay. Production of nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 was assessed by enzyme-linked immunosorbent assay. Real-time polymerase chain reaction and Western blot were performed to analyze mRNA and protein levels, respectively. Results: During the whole experiment, 15, 50, and 100 μg/mL of POG had no cytotoxicity on RAW 264.7 cells. POG dose-dependently inhibited the production of NO, TNF-α, IL-1β, and IL-6 that were induced by LPS. POG treatment downregulated the mRNA and protein expression inducible NO synthase (iNOS) and cyclooxygenase 2 (COX-2) in LPS-activated RAW 264.7 macrophages in a concentration-dependent manner. Furthermore, LPS-induced JAK2/STAT3 activation was prevented in RAW 264.7 macrophages by POG treatment. STAT3 overexpression significantly reversed the effects of POG on LPS-activated RAW 264.7 macrophages. Conclusion: These results demonstrate that POG exerts anti-inflammatory effects through the inhibition of iNOS and COX-2 expression by inhibiting the phosphorylation of JAK2/STAT3. Abbreviations used: LPS: Lipopolyssacharide; NO: Nitric oxide; TNF-α: Tumor necrosis factor-α; IL: Interleukin; RS: Radix Saposhnikoviae; POG: Prim-O-glucosylcimifugin; iNOS: Inducible NO synthase; COX2: Cyclooxygenase; FBS: Fetal bovine serum; DMSO: Dimethylsulfoxide; CCK-8: Cell Counting Kit; RIPA: Radio immunoprecipitation assay buffer; ECL: Enhanced chemiluminescence; SD: Standard deviation; ELISA: Enzyme-Linked immunosorbent assay. Dr. Hong Zhang,


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