Fig. 2: Inhibition of fatty acid synthesis ameliorated endotoxemia-induced lung injury and EC activation in vivo. | Cell Death & Differentiation

Fig. 2: Inhibition of fatty acid synthesis ameliorated endotoxemia-induced lung injury and EC activation in vivo.

From: Fatty acid synthesis promotes mtDNA release via ETS1-mediated oligomerization of VDAC1 facilitating endothelial dysfunction in sepsis-induced lung injury

Fig. 2

The C57BL/6N mice were i.p. injected with LPS (10 mg/kg) with or without C75 (10 mg/kg, i.p.) pretreatment for 1 h (n = 5). A–C The levels of TNF-α, IL-6, and TF in mice plasma were measured by ELISA (n = 5). D H&E staining showing the tissue injury in the lung (n = 5). E, F IHC staining showing the levels and distribution of VCAM-1 and E-selectin in the lung tissues (n = 5). G, H Immunofluorescent staining showing the levels of fibrinogen (anti-fibrinogen, Red) in lungs from septic mice pretreated with or without C75 (n = 5). CD31 (anti-CD31, Green) was used to label endothelial cells and nuclei were stained in blue with DAPI. I, J Immunoblot showing the expression levels of VCAM-1, E-selectin, PAI-1, and TF in the lung tissues in mice (n = 3). All data were expressed as the mean ± SD. Comparison among three or more groups was analyzed by one-way ANOVA. ns no significance, *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.

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