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. 2022 Sep 1;2022:4722647. doi: 10.1155/2022/4722647

Figure 5.

Figure 5

CypD-K166 acetylation is necessary for SNI-induced mitochondrial dysfunction and oxidative stress. (a, b) Open levels of mitochondrial permeability transition pore (mPTP) were evaluated by Flow Cytometry. Mean fluorescence intensity (MFI) is negatively correlated with mPTP opening (n = 6. ∗∗P < 0.01 vs Sham). (c) Mitochondrial Membrane Potential (MMP) in SNI model mice (n = 6. ∗∗P < 0.01 vs Sham). (d) Reactive oxygen species (ROS) levels in SNI model mice (n = 6. ∗P < 0.05 vs Sham). (e, f) Western blotting analysis for MnSOD levels (n =8. ∗∗P < 0.01 vs Sham). (g) MDA levels in SNI model mice (n = 6. ∗∗P < 0.01 vs Sham). (h–n) Changes in mPTP, MMP, ROS, MnSOD, and MDA levels in CypD-K166R point mutant mice after SNI surgery (n = 6-8. ∗∗P < 0.01 vs Sham-WT; ##P < 0.01 vs SNI-WT). All data are expressed as mean ± SD.