Research Paper Volume 12, Issue 13 pp 12869—12895
miR-183-5p alleviates early injury after intracerebral hemorrhage by inhibiting heme oxygenase-1 expression
Figure 5. miR-183-5p alleviated early inflammation and oxidative damage by directly targeting heme oxygenase-1 (HO-1). (A) Above: schematic showing the potential miR-183-5p binding site in the HO-1 3’-untranslated region (3’-UTR). A mutant (MUT) HO-1 3’-UTR was introduced by replacing the wild type (WT) binding sequence with a mutant sequence. Below: inhibition of relative luciferase activity of HO-1 3’-UTR reporter molecules in human embryonic kidney 293 cells mediated by miR-183-5p. miR-183-5p MM, miR-183-5p mimic; NC, nontarget control. (B) Above: western blotting revealed that miRNA-183-5p downregulated HO-1 expression. Below: quantitative analysis of HO-1 protein expression in different groups. n = 8/group. (C) Quantitative analysis of cytokine expression in the brains of mice from different groups pretreated with the HO-1 inhibitor zinc protoporphyrin IX (ZnPP) at 3 days after ICH. n = 8/group. (D) Quantitative analysis of 4-HNE expression in the brains of mice from different groups pretreated with the HO-1 inhibitor ZnPP at 3 days after ICH. n = 8/group. Values are presented as the mean ± standard deviation. *P < 0.05 vs. the ICH group.