Investigating CPT1A's Role in LPS-Induced ALI

ALI model of mice was induced as previously described^{43 (link)} via LPS (E. coli O111:B4; 5 mg/kg; Sigma-Aldrich, St. Louis, MO, USA) intratracheal injection (i.t.). Twelve hours after LPS treatment, the mice were sacrificed for further detection. To explore the role of CPT1A in ALI mice, mice were randomly divided into 4 groups: control, ALI, AAV-CPT1A, and ALI + AAV-CPT1A groups. Overexpression of CPT1A was administered by 1.5 × 10¹² genome copies (gc)/kg of AAV9 via tail-vein injection. The mice in the control group were treated with saline and the control AAV9. The ALI mice were treated with LPS and the control AAV9. To explore the role of CPT1A blocking on ALI mice, mice were randomly divided into 3 groups: control, ALI, and ALI + etomoxir groups. Mice in the ALI + etomoxir group received etomoxir (20 mg/kg; MedChemExpress, USA) via intraperitoneal injection 1 h before saline or LPS administration. For the survival study, mice were treated with LPS at a lethal dose (25 mg/kg, i.t.). Mice in the control group received saline only. The survival rate was monitored every 6 h.