Fig. 2: FABP4 inhibitor BMS309403 treatment alleviated CLP-induced septic AKI in mice. | Cell Death & Disease

Fig. 2: FABP4 inhibitor BMS309403 treatment alleviated CLP-induced septic AKI in mice.

From: Fatty acid-binding protein 4 is a therapeutic target for septic acute kidney injury by regulating inflammatory response and cell apoptosis

Fig. 2: FABP4 inhibitor BMS309403 treatment alleviated CLP-induced septic AKI in mice.

C57BL/6J and BMS309403 (BMS)-treated C57BL/6J mice (male, 8–10 weeks old) were subjected to CLP or sham surgery and killed 16 h later. A The mRNA expression of FABP4 in the kidneys analyzed by quantitative real-time PCR analysis (n = 3). B Protein expression of kidney FABP4 detected by western blotting and quantified by densitometry (n = 6). C Representative micrographs and quantitative analysis of immunochemistry staining of FABP4 in kidney tissue sections (×200, scale bar = 50 μm; ×400, scale bar = 20 μm). D Serum creatinine (Scr) and (E) BUN concentrations in different groups of mice (n = 6). F The mRNA expression of NGAL and KIM1 analyzed by quantitative real-time PCR analysis in kidney tissues (n = 3). G Representative images of HE staining (×200, scale bar = 50 μm; ×400, scale bar = 20 μm) and H tubular injury scores of kidney tissues (n = 6). Triangle: tubular dilatation; Asterisk: tubular swelling; Circle: cast formation; Arrow: loss of brush border. I Representative electron micrographs of renal tubular epithelial cells (RTECs) from different groups of mice (×8000, scale bar = 2 μm; ×12,000, scale bar = 1 μm; ×20,000, scale bar = 1 μm). Triangle: chromosome condensation; Asterisk: mitochondrial swelling; Circle: mitochondrial cristate fused; Arrow: mitochondrial cristate disappeared. Data are shown as mean ± SD; ****P < 0.0001, versus Sham; ####P < 0.0001, versus CLP.

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