Fig. 6

Data indicates that mitochondrial dysfunction occurs as a result of damage induced by 6-OHDA. Importantly, co-treatment with exendin-4 (Ex4) exhibits a protective effect against the loss of mitochondrial function in N27 cells. A N27 cells were incubated for 18 hours with or without 30 µM of 6-OHDA and/or 50 nM Ex4. Subsequently, extracellular flux analysis was performed. Oxygen consumption rate (OCR) was measured sequentially after the injection of 25 mM glucose and a set of mitochondrial inhibitors (1 µM oligomycin, 1 µM FCCP, and 0.5 µM each of rotenone and antimycin A) to generate a mitochondrial stress profile. (B–G) Mitochondrial parameters were calculated from the mitochondrial stress profile using the methods described in this study. The parameters assessed were: B basal respiration, C maximal respiration, D mitochondrial ATP turnover, E reserve capacity, F proton leak and G non-mitochondrial OCR. One-way analysis of variance (ANOVA) followed by Bonferroni post hoc test for multiple comparisons. Control vs Control + Ex-4 or 6-OHDA or 6-OHDA + Ex-4: *, p < 0.01; **, p < 0.05; ***, p < 0.001; 6-OHDA vs 6-OHDA+ Ex-4: #, p < 0.01; ##, p < 0.05; ###, p < 0.001. (N = 6)