Pctr1

Mice were intraperitoneally injected with LPS (15 mg/kg, Escherichia coli, serotype 055: B5; Sigma, Saint Louis, MO, USA) for survival experiments and LPS (10 mg/kg) for other experiments. The effect of PCTR1 (Cayman Chemical, Ann Arbor, MI, USA) on LPS-induced sepsis model was determined by establishing four experimental groups: control group, LPS group, LPS + PCTR1 group (LPS and PCTR1 were given simultaneously), PCTR1 group. For the PCTR1 and the control groups, the mice were intraperitoneally injected with PCTR1 100 ng/mouse or an equal saline volume. Next, to determine the mechanism of PCTR1, four groups were established: control group, LPS group, LPS + PCTR1 group, LPS + PCTR1 + BOC-2 group, LPS + PCTR1 + EX527 group, and LPS + BAY11-7082 group. Mice were administered with BOC-2 (600 ng/kg, Biomol-Enzo Life Sciences, Farmingdale, NY), EX527 (10 mg/kg, MEC, Shanghai, China), and BAY11-7082 (20 mg/kg, Selleck, Houston, TX, USA) intraperitoneally following LPS administration. The mice were anesthetized with 1% pentobarbital and sacrificed 6 h later. We obtained blood samples via the ophthalmic artery from mice that survived in each group, and obtained lung specimens.

PCTR1 (16-glutathionyl,17-hydroxy-4Z,7Z,10,12,14,19Z-docosahexaenoic acid) and H89 (PKA antagonist) were purchased from Cayman Chemical (Ann Arbor, MI). LPS (Escherichia coli 055: B5) and ferrostatin-1(ferroptosis antagonist) were purchased from Sigma (St. Louis, MO, USA). 1S,3R-RSL3 (ferroptosis agonist), 666-15 (CREB antagonist), MCC950 (pyroptosis antagonist) and Necrostatin-1 (necroptosis antagonist) were obtained from Med Chem Express (New Jersey, USA). BOC-2 (ALX receptor inhibitor) was purchased from Biomol-Enzo Life Sciences (Farmingdale, NY).