Figure 7.

Silencing lncRNA AAB by NM + si-AAB + MSN inhibits cardiac hypertrophy

(A) Scheme of time axis showing the design of animal study. (B and C) Detection of ICAM-1 protein expression by western blot analysis at different time points of AAC. (D) Images of hearts with fluorescent signals of MSN after tail vein injection of PBS, si-AAB, si-AAB+MSN, and NM+si-AAB+MSN, respectively. (E) Electron microscopy was used to observe morphological changes of mitochondria in CMECs. (F) Gelatin ink was injected into hearts after tail vein injection of PBS, si-AAB, si-AAB+MSN, and NM+si-AAB+MSN for 4 weeks, respectively, and samples were observed via microscope. (G) Typical images of the echocardiography in different groups. (H–I) The echocardiographic parameters including LVFS and LVEF were measured. (J and K) Representative sections of hearts stained for HE and WGA staining. (L and M) Detection of BNP and β-MHC protein expression by western blot analysis in cardiac tissue of rats. Model group: rats were subjected to AAC and received vehicle (PBS, caudal vein injection) 24 h later once every 2 days for 4 weeks. si-AAB group: rats were subjected to AAC and treated with si-AAB via tail vein injection 24 h later every 2 days for 4 weeks. si-AAB+MSN group: rats were subjected to AAC and treated with si-AAB+MSN via tail vein injection 24 h later every 2 days for 4 weeks. NM+si-AAB+MSN group: rats were subjected to AAC and treated with NM + si-AAB + MSN via tail vein injection 24 h later every 2 days for 4 weeks. Data are represented by means ± SEM (n=6). ^##p <0.01 versus sham group; ^∗∗p <0.01 versus model group. Scale bars, (E) 1.0 μm; (F) 200 μm (×100); 100 μm (×200); (J) 50 μm.