Figure 5
From: CPT1A as a potential therapeutic target for lipopolysaccharide-induced acute lung injury in mice
CPT1A overexpression mitigated mitochondrial dysfunction and restored FAO in lung tissue of ALI mice and LPS-treated MLE12 cells. (A) Mitochondrial DNA copy number (mtDNA) was determined in the lungs. (B) Radiolabeled palmitate-derived CO2 was determined after incubating 14C-palmitate with lung tissue after doxycycline induction. (C) ATP levels in total lung tissue. (D) Peroxisomal/mitochondrial function-associated genes were determined in the lungs after doxycycline induction. (E) OCR of MLE12 cells was measured with a Seahorse XF24 Extracellular Flux Analyzer. Bar graphs show the rates of OCR associated with basal, proton-leak, ATP-linked, maximum, reserve capacity, and nonmitochondrial respiratory statuses. (F) Extracellular acidification rate (ECAR) of MLE12 cells. (G) ATP levels of MLE12 cells. n = 6, *P < 0.05, **P < 0.01, and ***P < 0.001.
