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. 2020 Oct 14;22(6):5095–5104. doi: 10.3892/mmr.2020.11601

Figure 4.

Figure 4.

HULC knockdown ameliorates LPS-induced apoptosis and inflammation in HMEC-1 cells by targeting miR-128-3p. (A) miR-128-3p expression in HMEC-1 cells treated with LPS or DMSO (control). (B) miR-128-3p expression levels in HMEC-1 cells transfected with anti-miR-NC or anti-miR-128-3p. (C-F) HMEC-1 cells treated with LPS were transfected with anti-miR-NC, anti-miR-128-3p, si-HULC + anti-miR-NC or si-HULC + anti-miR-128-3p. (C) Apoptotic rate of transfected HMEC-1 cells. (D) Protein expression levels of cleaved-cas3 and cleaved-cas9 in transfected HMEC-1 cells. The (E) mRNA and (F) protein expression levels of IL-6, TNF-α, ICAM1 and VCAM1 in transfected HMEC-1 cells. *P<0.05. **P<0.01. HULC, highly upregulated in liver cancer; LPS, lipopolysaccharide; miR, microRNA; NC, negative control; siRNA, small interfering RNA; ICAM1, intercellular adhesion molecule; VCAM1, vascular cell adhesion molecule; DMSO, dimethyl sulfoxide; HMEC-1, human dermal microvascular endothelial cells; cas, caspase.