Skip to main content
. 2016 Jul 27;6:30377. doi: 10.1038/srep30377

Figure 1. Hepatotoxicity of gapmer and ‘non-gapmer’.

Figure 1

(a) Schematic illustration of a gapmer and non-gapmer. The non-gapmer was designed to reduce gapmer activity by substituting two naïve deoxyribonucleotides for LNA at the centre of the gap. Plasma ALT (b), AST (c) levels in mice received 10 mg/kg of GR ASO were analysed at 4, 7 and 10 days after administration. Whole liver weight (d) and GR mRNA level (e) were measured on day 10. The same experiments were performed with Acsl1 gapmer and non-gapmer (20 mg/kg): plasma ALT (f), AST (g), liver weight (h) Acsl1 mRNA level (i), and mRNA level of IFNγ, TNFα, IL6 (j). (n = 4, mean ± S.D. *p < 0.05, Mann–Whitney U test, vs saline).