Fig. 9

Exogenous delivery of miR-124 could inhibit the expression of MEKK3 and p-p65 in the SNpc of MPTP-treated mice in vivo. The mice were treated with stereotactic intraventricular treatment of miR-124 agomir for five consecutive days. Next, the mice received one intraperitoneal injection of MPTP-HCl per day for 5 days, while the control mice received saline injections. Agomir treatment was performed 2 days prior to the injection of MPTP. Then, the mice were decapitated, and the midbrains were obtained 7 days after the last MPTP injection. a The miR-124 expression was evaluated using RT-qPCR and normalised with U6 RNA. In the agomir-treated mice and their negative control counterparts on day 7 after the last injection of MPTP, RT-qPCR was used to determine the production mRNA levels of MEKK3 (b), and western blot analysis was used to evaluate the MEKK3 (c) expression in total protein samples extracted from the midbrain. The fold change was normalised by GAPDH levels. Immunohistochemical analysis was performed to analyse the MEKK3 response (d), and a graphical representation of MEKK3 IOD value (e) from the midbrain is shown. The scale bar represents 50 μm. f Western blot analysis was used to determine the p-p65 protein expression. Data are normalised to saline controls and presented as the mean ± SD of three independent experiments. The fold change is statistically significant. *P < 0.05, **P < 0.01