过氧化物酶体增殖物激活受体γ配体15-脱氧（δ12,14）前列腺素J2可减轻内毒素休克中的肝损伤。
The PPAR-gamma ligand 15-deoxy(delta12,14) prostaglandin J2 reduces the liver injury in endotoxic shock.
作者信息
Collin Marika, Thiemermann Christoph
机构信息
Department of Experimental Medicine and Nephrology, The 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. 2003 Aug 29;476(3):257-8. doi: 10.1016/s0014-2999(03)02179-4.
We demonstrate here for the first time that the endogenous cyclopentenone prostaglandin 15-deoxy-Delta12,14-prostaglandin J2 (15d-prostaglandin J2) reduces the liver injury (rise in serum transaminases) caused by severe endotoxaemia (6 mg/kg Escherichia coli endotoxin i.v. for 6 h) in the anaesthetised rat. The protection of the liver afforded by this potent agonist of PPAR-gamma was not secondary to a haemodynamic effect. Thus, 15d-prostaglandin J2 and other PPAR-gamma agonists may be useful in the therapy of septic shock.
我们首次在此证明，内源性环戊烯酮前列腺素15-脱氧-Δ12,14-前列腺素J2（15d-前列腺素J2）可减轻麻醉大鼠因严重内毒素血症（静脉注射6 mg/kg大肠杆菌内毒素，持续6小时）所致的肝损伤（血清转氨酶升高）。这种PPAR-γ强效激动剂对肝脏的保护作用并非继发于血流动力学效应。因此，15d-前列腺素J2和其他PPAR-γ激动剂可能对脓毒性休克的治疗有用。
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