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. 2018 Jan 1;8(4):1027–1041. doi: 10.7150/thno.22414

Figure 6.

Figure 6

Cardiac-specific ALDH2 upregulation in vivo enhances ALDH2 activation and ameliorates cardiac protein carbonylation. (A) Representative western blot analysis and quantification of protein levels of cardiac ALDH2 expression in AAV9-cTNT-ALDH2-injected mice or negative controls injected with AAV9-cTNT-GFP; *P < 0.05 vs. no-AAV control (B) Immunoblot results show ALDH2 was specifically upregulated in the mouse heart after AAV9-cTNT-ALDH2 treatment. (C) Immunohistochemical analysis was performed to confirm the cardiac-specific ALDH2 upregulation vs. DRG (scale bar, 20 μm). (D) Representative immunoblots and quantification of protein levels of ALDH2 expression in the heart and DRG from AAV9-cTNT-ALDH2- and AAV9-cTNT-GFP-exposed mice; *P < 0.05 vs. AAV9-cTNT-GFP-injected heart. (E) Protocol for ALDH2 gene therapy in mouse model. CCD surgery was performed, followed 2 weeks later by ex vivo I/R by Langendroff perfusion in AAV9-cTNT-ALDH2-injected mice or AAV9-cTNT-GFP-injected mice. (F) Cardiac ALDH2 activation. (G) Representative analysis of cardiac protein carbonyl level. (H) Ipsilateral nociceptive threshold and (I) plasma 4-HNE levels in rAAV9-ALDH2-injected CCD mice or rAAV9-LacZ-injected CCD mice compared to the no pain control mice; *P < 0.05 vs.no-AAV9 control; #P < 0.05 vs. AAV9-cTNT-GFP-injected heart. Values are mean ± SEM, n = 6 per group.