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10.1007/s10753-015-0140-2

http://scihub22266oqcxt.onion/10.1007/s10753-015-0140-2
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25691139!ä!25691139

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suck abstract from ncbi


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pmid25691139      Inflammation 2015 ; 38 (4): 1639-48
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  • Anti-inflammatory Activity of Magnesium Isoglycyrrhizinate Through Inhibition of Phospholipase A2/Arachidonic Acid Pathway #MMPMID25691139
  • Xie C; Li X; Wu J; Liang Z; Deng F; Xie W; Zhu M; Zhu J; Zhu W; Geng S; Zhong C
  • Inflammation 2015[Aug]; 38 (4): 1639-48 PMID25691139show ga
  • Glycyrrhiza glabra (licorice) has been known to possess various pharmacological properties including anti-inflammatory, antioxidants, antiviral, and hepatoprotective activities. Magnesium isoglycyrrhizinate (MgIG), a magnesium salt of 18-alpha glycyrrhizic acid stereoisomer, is clinically used for the treatment of inflammatory liver diseases. However, the mechanism by which MgIG exerts its anti-inflammatory effects remains unknown. In the present study, we investigated the inhibitory potential of MgIG in phospholipase A2 (PLA2)/arachidonic acid (AA) pathway and release of the pathway-generated inflammatory lipid mediators in RAW264.7 macrophages. Results revealed that MgIG suppressed LPS-induced activation of PLA2 and production of AA metabolites such as prostaglandin E2 (PGE2), prostacyclin (PGI2), thromboxane 2 (TXB2), and leukotrienes (LTB4) in macrophages. Furthermore, LPS-induced AA-metabolizing enzymes including COX-2, COX-1, 5-LOX, TXB synthase, and PGI2 synthase were significantly inhibited by MgIG. Taken together, our data suggest that modulation of cyclooxygenase (COXs) and 5-lipoxygenase (LOX) pathways in AA metabolism could be a novel mechanism for the anti-inflammatory effects of MgIG.
  • |Animals[MESH]
  • |Anti-Inflammatory Agents/*pharmacology[MESH]
  • |Arachidonic Acid/antagonists & inhibitors/*metabolism[MESH]
  • |Cell Line[MESH]
  • |Drugs, Chinese Herbal/*pharmacology[MESH]
  • |Macrophages/drug effects/metabolism[MESH]
  • |Mice[MESH]
  • |Phospholipases A2/*metabolism[MESH]
  • |Saponins/*pharmacology[MESH]
  • |Signal Transduction/*drug effects/physiology[MESH]


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