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. 2020 Aug 18;11:1281. doi: 10.3389/fphar.2020.01281

Figure 6.

Figure 6

NLRC5 inhibits inflammation in EESCs by promoting autophagy (n = 9). (A–C) Representative western blotting, qRT-PCR, and ELISA showing promotion of autophagy by using 1 nM autophagy agonist rapamycin significantly inhibited IL-6 and TNF-α expression when compared with control group (**P < 0.01 vs. control group). (D–F) Representative western blotting, qRT-PCR, and ELISA showing inhibition of autophagy by using 30 μM autophagy inhibitor CQ significantly promoted IL-6 and TNF-α expression when compared with control group (**P < 0.01 vs. control group). (G–I) Representative western blotting, qRT-PCR, and ELISA showing promotion of autophagy by 1 nM rapamycin contributed to the NLRC5-mediated inhibition of IL-6 and TNF-α expression in EESCs (**P < 0.01 vs. vector group and ##P < 0.01 vs. NLRC5 group). (G) Representative western blotting, qRT-PCR, and ELISA showing inhibited autophagy by 30 μM CQ restricted the NLRC5-mediated inhibition of IL-6 and TNF-α expression in EESCs (**P < 0.01 vs. vector group and ##P < 0.01 vs. NLRC5 group). The expression levels of mRNA were normalized with respect to β-actin and were calculated using the 2-ΔΔCt method. The protein expression levels were quantified by Image J software and normalized to β-actin protein levels. The results are represented as the mean ± SEM from at least three independent experiments.