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. 2020 Feb 17;16(8):1303–1323. doi: 10.7150/ijbs.38962

Figure 3.

Figure 3

Figure 3

Figure 3

Figure 3

ALDH2 overexpression alleviated MCAO-induced mitochondrial dysfunction and mitochondria-relative apoptosis. A. ALDH2 overexpression preserved the stability of mitochondrial electrochemical gradient (ΔΨm); B. ALDH2 overexpression inhibited mitochondrial permeability transition pore (mPTP) opening; C. ALDH2 overexpression suppressed mitochondrial ROS generation; D. Release of Cyt-C from the mitochondria to cytoplasm; E. The relative release rate of Cyt-C from the mitochondria to cytoplasm; F. Selected plots of active caspase-9 and -3 in different groups; G. Relative optical density of active caspase-9 and -3. H. Selected plots of Bcl-2 and Bax expression in mitochondria in different groups; I. Relative ratio density of Bcl-2/Bax in mitochondria. J. Phosphorylated JNK (p-JNK) and JNK expression in different groups; K. Relative optical density of p-JNK and JNK; L -O. Coronal sections of the ischemic penumbra of MCAO rats with or without treatment of lentivirus overexpressing ALDH2. These were immunostained with an anti‐p-JNK (red) and an anti-Neun or an anti‐glial fibrillary acidic protein (GFAP, green), Magnification, 400×, Scale bar: 100 μm. P and Q. Immunoprecipitation and immunoblotting assays showing p-JNK and caspase-3 binding after transient MCAO. Mean ± SD was used to describe the data (n = 6-8 in each group). # indicated P < 0.05.