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. 2021 Aug 8;46:102095. doi: 10.1016/j.redox.2021.102095

Fig. 2.

Fig. 2

IGF-II protects mitochondrial function and integrity in SN4741 dopaminergic cells against MPP+-induced toxicity in cell cultures. (A) Experimental design for the study of the neuroprotective effects of IGF-II on mitochondrial integrity, function, and redox homeostasis. The measures were taken in SN4741 cells after 2.5 h of incubation with MPP+, in the presence or absence of IGF-II and/or BMS and AB. (B) OCR time course after treatments expressed as % of the control. (C) Electronic microscopy. (D) Mitochondrial ROS production evaluated as MitoSOX fluorescence. (E) Mitochondrial mΔΨ evaluated as JC1 fluorescence aggregates; BMS is used to define the receptor involved in the IGF-II effect. (F) Mitochondrial COX activity; AB is used to define the receptor involved in the IGF-II effect. (G) Mitochondrial SOD activity; AB is used to define the receptor involved in the IGF-II effect. (H) Representative immunocytochemistry of DAPI, TFAM, and MTR mitochondrial stain. (I) Quantification of TFAM immunofluorescence; AB is used to define the receptor involved in the IGF-II effect. Data are expressed as mean ± SEM. n = 6 each group (3 independent experiment). #P < 0.05 versus CO and IGF-II groups; *P < 0.05, versus groups connected in bars; & P < 0.05, versus all other groups. Data were analysed by one-way ANOVA followed by Tukey's multiple comparison test.