过氧化物酶体增殖物激活受体γ的内源性配体可减轻失血性休克中的肝损伤。
Endogenous ligands of PPAR-gamma reduce the liver injury in haemorrhagic shock.
作者信息
Collin Marika, Abdelrahman Maha, Thiemermann Christoph
机构信息
Department of Experimental Medicine and Nephrology, William Harvey Research Institute, St. Bartholomew's and The Royal London School of Medicine and Dentistry, Charterhouse Square, London EC1M 6BQ, UK.
出版信息
Eur J Pharmacol. 2004 Feb 20;486(2):233-5. doi: 10.1016/j.ejphar.2003.12.032.
We demonstrate here for the first time that the novel, potent peroxisome proliferator-activated receptor (PPAR)-gamma antagonist GW9662 (2-chloro-5-nitrobenzanilide) augments the degree of liver injury associated with haemorrhagic (haemorrhage for 90 min and resuscitation for 4 h), but not endotoxic (6 mg/kg E. coli endotoxin i.v. for 6 h) shock in the anaesthetised rat. Thus, endogenous ligands for PPAR-gamma are released in haemorrhagic, but not endotoxic, shock in sufficient amounts to protect against injury.
我们首次在此证明，新型强效过氧化物酶体增殖物激活受体（PPAR）-γ拮抗剂GW9662（2-氯-5-硝基苯甲酰苯胺）会加剧麻醉大鼠与出血性休克（出血90分钟并复苏4小时）相关的肝损伤程度，但不会加剧与内毒素性休克（静脉注射6 mg/kg大肠杆菌内毒素6小时）相关的肝损伤程度。因此，PPAR-γ的内源性配体在出血性休克而非内毒素性休克中会大量释放，足以起到保护作用，防止损伤。
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