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. 2018 Jan 10;9(19):14959–14976. doi: 10.18632/oncotarget.24127

Figure 6. FC-99 increased the expression of let-7a-5p that inhibited the expression of its target gene BCL-XL.

Figure 6

(A) qRT-PCR evaluation of the expression levels of let-7a-5p and its target gene BCL-XL in response to FC-99 (10 mg/k, i.p.) in the septic liver at 24 h. (B) LPS (100 ng/mL) was applied in order to induce inflammation in vivo. THP-1 cells were pre-treated with FC-99 (10 μM) and/or vehicle 2 h prior to the addition of LPS for another 24 h. The expression levels of let-7a-5p and BCL-XL mRNA were detected by qRT-PCR. (C) THP-1 cells were transfected with let-7a-5p mimic (50 nM final concentration) for 24 h, followed by the addition of FC-99 (10 μM) for another 24 h in order to determine the effects of let-7a-5p on FC-99. (D) THP-1 was transfected with let-7a-5p inhibitor (50 nM final concentration) for 24 h, and subsequently with FC-99 (10 µM) for another 24 h in order to determine the effects of FC-99 on let-7a-5p. The expression levels of let-7a-5p and BCL-XL were assessed by qRT-PCR. *P < 0.05, **P < 0.01, ***P < 0.005, vs. sham operation group in vivo and/or vs. control group in vitro; #P < 0.05, ##P < 0.01, ### P < 0.005, vs. CLP group and/or vs. LPS group and/or vs. let-7a inhibitor group in vitro, &P < 0.05, &&P < 0.01, &&&P < 0.005, vs. NC-inhibitor+FC-99 group in vitro.