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

Figure 4.

Figure 4

ALDH2 activation reduces nociception and aldehydic load in CCD mice. (A) Nociceptive threshold in no-CCD WT control or WT mice 2 weeks post-CCD with or without Alda-1 (ALDH2 selective activator) treatment (3 mg/kg BW per injection, 3 doses per day for 2 weeks); *P < 0.05 vs. no-CCD WT control; #P < 0.05 vs. CCD alone. (B) Alda-1 treatment-induced anti-nociceptive effect is independent of opioid receptor pathway (Naloxone, opioid receptor antagonist, 1mg/kg per subcutaneous injection give 10 min prior to Alda-1 treatment); *P < 0.05 vs. CCD alone. (C) Plasma 4-HNE level. (D) Cardiac ALDH2 activity. (E) Cardiac protein carbonyl levels. (F) Representative co-immunoprecipitation analysis of carbonylation of SIRT1 and acetylation of LKB1 and (G) SIRT1 activity in the cardiac tissue from no pain WT control or 2 weeks post-CCD with or without Alda-1 treatment groups; *P < 0.05 vs. no pain control; #P < 0.05 vs. CCD alone. (H) Immunoblots of AMPKα from LKB1 immune-complexes and (I) immunoblots of p-AMPKα (Thr 172) and p-ACC (Ser 79) during sham or ischemic conditions (ischemia 10 min, in vivo) in no pain WT control or 2 weeks post-CCD with or without Alda-1 treatment groups. Bar graphs show the ratio of phosphorylated to total AMPK; *P < 0.05 vs. CCD vehicle sham; #P < 0.05 vs. CCD vehicle MI. Values are mean ± SEM, n = 6 per group.