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. 2020 Jan 20;18(1):69. doi: 10.3390/md18010069

Figure 5.

Figure 5

COS inhibits lipogenesis via suppression of SMYD3 and HMGCR in vitro. The high steatosis model of HepG2 liver cells was established by oleic acid induction, and the lipid accumulation was determined by oil red (O) staining (A). The mRNA and protein levels of HMGCR and SMYD3 and the transcriptional activity of HMGCR promoter during the oleic acid-induced lipid accumulation were detected by RT-qPCR (B), Western blotting (C), and luciferase reporter assay (D), respectively. Effects of RNA interference (RNAi)-mediated suppression of endogenous SMYD3 on the oleic acid-induced upregulation of HMGCR and SMYD3 were also examined (E–G). Furthermore, effects of SMYD3 overexpression and COS treatment on the transcriptional activity of HMGCR promoter (H), mRNA (I), and protein (J) levels of SMYD3 and HMGCR were also detected. Data are presented as mean ± SD (n = 8); In (B,D), * p < 0.05 and ** p < 0.01, compared with control group (NC); # p < 0.05 and ## p < 0.01, compared with oleic acid-treated group (HF); In (E,F), * p < 0.05 and ** p < 0.01, compared with control siRNA-treated group (si-control or si-control + OA). In (H,I), * p < 0.05 and ** p < 0.01, compared with pcDNA 3.1 transfected group (NC), # p < 0.05 and ## p < 0.01, compared with SMYD3 transfected group (OA).