Skip to main content
. 2016 May 3;7(22):31708–31722. doi: 10.18632/oncotarget.9150

Figure 4. Effect of DCA treatment on brain mitochondrial fission and fusion.

Figure 4

A. The mRNA expression levels of the mitochondrial fusion (Mfn1, OPA1) and fission (Drp1) genes in the mouse brain were quantified by RT-qPCR at 6 h after HI. B. The mRNA expression levels of the mitochondrial fusion (Mfn1, OPA1) and fission (Drp1) genes in the mouse brain were quantified by RT-qPCR at 24 h after HI. n = 5 for the vehicle control, n = 6 for the DCA control at 6 h, n = 6 for the 6 h HI and 6 h DCA groups; n = 6 for the vehicle control, n = 7 for the DCA control at 24 h, n = 8 for the 24 h HI vehicle group, and n = 7 for the 24 h HI DCA group. C. Immunoblotting of OPA1, MFN1, and P-DRP1 in the mitochondrial fraction of normal control (Cont) and 6 h after HI treated with vehicle (Veh) or DCA. The 90 kDa upper band of OPA1 was decreased significantly at 6 h after HI, and DCA treatment did not prevent the reduction (n = 6/group). D. Immunobloting of OPA1, and P-DRP1 in normal controls and 24 h after HI treated with vehicle or DCA. The expression of these proteins decreased significantly at 24 h after HI in the mitochondrial fraction. The 75 kDa cleavage band of OPA1 increased significantly after HI, and DCA treatment has no significant effect on OPA1 cleavage at 24 h after HI (n = 6/group). *p < 0.05, **p < 0.01.