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. 2022 Apr 11;13(4):333. doi: 10.1038/s41419-022-04794-w

Fig. 3. Genetic or pharmacologic inhibition of FABP4 alleviated CLP-induced kidney inflammation and apoptosis in mice.

Fig. 3

C57BL/6J, FABP4 inhibitor BMS309403 (BMS)-treated C57BL/6J, FABP4 KO, and WT mice (male, 8–10 weeks old) were subjected to CLP or sham surgery and killed 16 h later. A The mRNA levels of inflammatory cytokines including IL-1β, IL-6, TNF-α, and MCP-1 in kidney tissues measured by quantitative real-time PCR (n = 3). B The protein levels of inflammatory cytokines including IL-1β, IL-6, TNF-α, and MCP-1 in the kidneys examined by western blotting and quantified by densitometry (n = 6). C The mRNA levels of apoptotic markers including Bcl-2 and Bax in renal tissues measured by quantitative real-time PCR (n = 3). D The protein levels of apoptotic markers including Bcl-2, Bcl-XL, Bax, Caspase 3 (Cas 3), and cleaved-caspase 3 (C-Cas 3) in the kidneys analyzed by western blotting and quantified by densitometry (n = 6). E Representative images of TUNEL staining (×200, scale bar = 50 μm) and quantification of TUNEL-positive cells in kidney cortex (n = 6). All data are represented as mean ± SD; ***P < 0.001, ****P < 0.0001 for WT CLP versus WT Sham, or for CLP versus Sham; #P < 0.05, ##P < 0.01, ###P < 0.001, ####P < 0.0001 for FABP4-KO CLP versus WT CLP, or for CLP + BMS versus CLP.