Fig. 4: STN-DBS alleviates oxidative stress and stabilizes mitochondrial homeostasis.

a, b SOD and GSH levels in SN measured via ELISAs. An increased expression of SOD and GSH in SN, compared with the mice that received no stimulation or rapamycin (only SOD) injection. The mTOR activator 3BDO inhibited this effect (n = 6 per group; SOD: F_(5,30) = 22.6, P < 0.0001; GSH: F_(5,30) = 13.6, P < 0.0001; one-way ANOVA followed by a Tukey post-hoc correction). c Complex I activity in SN measured via ELISAs. Complex I had higher activity in PD mice that received STN stimulation or rapamycin treatment, however, the mTOR activator could suppress the effect of STN stimulation on the activity of complex I (n = 6 per group; F_(5,30) = 44.0, P < 0.0001; one-way ANOVA followed by a Tukey post-hoc correction). d Western blot analysis of Drp1 and Opa1 in mitochondria of SN. e, f Opa1 expression in mitochondria was decreased in PD mice, whereas, an elevated expression of Opa1 was detected in PD mice treated with STN stimulation (n = 6 per group; F_(3,20) = 26.3, P < 0.0001; one-way ANOVA followed by a Tukey post-hoc correction). On the contrary, the opposite trend of Drp1 expression was observed in the mitochondria of SN (n = 6 per group; F_(3,20) = 74.6, P < 0.0001; one-way ANOVA followed by a Tukey post-hoc correction). I: control group; II: PD group; III: PD-sham-DBS group; IV: PD-DBS group; V: PD+Rap group; VI: PD-DBS + 3BDO group. ^*P < 0.05; ^**P < 0.01; ^***P < 0.001; ^****P < 0.0001. Error bars: standard deviation of the mean. STN-DBS subthalamic nuclei deep brain stimulation, PD Parkinson’s disease, SN substantia nigra, ELISA enzyme-linked immunosorbent assay, SOD superoxide dismutase, GSH glutathione, ns not significant.