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

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Copyright: © Yang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 2. — Silencing of HULC partially reverses LPS-induced apoptosis and inflammation in a cell model of sepsis. (A) HULC expression levels in HMEC-1 cells treated with LPS or DMSO (control). (B) HULC expression in HMEC-1 cells transfected with si-HULC or si-NC. (C-F) HMEC-1 cells treated with LPS or DMSO (control) were transfected with si-HULC or si-NC. (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<0.01. HULC, highly upregulated in liver cancer; ICAM1, intercellular adhesion molecule; VCAM1, vascular cell adhesion molecule; siRNA, small interfering RNA; NC, negative control; LPS, lipopolysaccharide; HMEC-1, human dermal microvascular endothelial cells; DMSO, dimethyl sulfoxide; cas, caspase.