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10.1016/j.clim.2020.108461

http://scihub22266oqcxt.onion/10.1016/j.clim.2020.108461
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32437924!ä!32437924

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suck abstract from ncbi


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pmid32437924      Clin+Immunol 2020 ; 216 (ä): 108461
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  • Hydroxychloroquine inhibiting neutrophil extracellular trap formation alleviates hepatic ischemia/reperfusion injury by blocking TLR9 in mice #MMPMID32437924
  • Zhang S; Zhang Q; Wang F; Guo X; Liu T; Zhao Y; Gu B; Chen H; Li Y
  • Clin Immunol 2020[Jul]; 216 (ä): 108461 PMID32437924show ga
  • Hepatic ischemia/reperfusion (I/R) injury may arise after partial hepatectomy and liver transplantation. Neutrophil extracellular traps (NETs) were involved in hepatic I/R injury. This study tested the hypothesis that blocking NETs formation could be a potential therapeutic target against hepatic I/R injury. NETs were excessively formed within liver and in serum of I/R mice models and were testified to be an independent contributor to hepatic I/R injury. Hydroxychloroquine (HCQ) alleviated hepatic I/R injury by inhibiting NETs formation in SCID and c57BL/6 mice models. In vitro, HCQ inhibited neutrophils to form NETs at a concentration of 100 mug/ml. CpG-ODN reversed the effect of HCQ inhibiting NETs formation. HCQ inhibited PAD4 and Rac2 expressions by blocking TLR9. NETs are essential contributors to hepatic I/R injury. HCQ blocking TLR9 protects against hepatic I/R injury by inhibiting NETs formation, which may suggest utility of HCQ or other TLR9 agonists for preventing hepatic I/R injury in clinical practices.
  • |Animals[MESH]
  • |Disease Models, Animal[MESH]
  • |Extracellular Traps/*drug effects/metabolism[MESH]
  • |Hydroxychloroquine/*pharmacology[MESH]
  • |Liver/*drug effects/metabolism[MESH]
  • |Male[MESH]
  • |Mice[MESH]
  • |Mice, Inbred C57BL[MESH]
  • |Mice, SCID[MESH]
  • |Neutrophils/*drug effects/metabolism[MESH]
  • |Protein-Arginine Deiminase Type 4/metabolism[MESH]
  • |RAC2 GTP-Binding Protein[MESH]
  • |Reperfusion Injury/*drug therapy/*metabolism[MESH]
  • |Toll-Like Receptor 9/*metabolism[MESH]


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