Effect of LL-ES of ARVGP on protein expression in the LV
After 1w of drug administration, the TGF-β expression down-regulated from 1.2±0.12 in the control group to 0.99±0.06 (P =0.001, n=10, Figure 3), levels of MMP-9 decreased from 1.37±0.13 to 1.13±0.12(P =0.001, n=10, Figure 3), and AT-1R reduced from1.20±0.73to 0.99±0.15(P =0.001, n=10, Figure 2).While levels of p-ERK1/2were not significantly different compared to the control group(1.14±0.15vs.1.12±0.13; P =0.79, n=10, Figure 3). However, TGF-β protein levels in the LL-ES group decreased significantly from 0.99±0.06 to 0.44±0.07 compared to the drug group, MMP-9 down-regulated significantly from 1.13±0.13 to 0.24±0.07(P =0.001, n=10, Figure 3), and AT-1R reduced significantly from 0.99±0.15 to 0.67±0.10 (P =0.001, n=10, Figure 3). To explore potential signaling pathways by which LL-ES mediated cardiomyocyte protection, p-ERK1/2 was measured. p-ERK1/2 is a well-known stress-activated MAPK that plays a protective role in the cell death signaling pathway. As shown in Figure 2, p-ERK1/2 increased significantly from 1.14±0.15 in the drug group to 2.09±0.13 after LL-ES (P =0.001, n=10, Figure 3). In this figure, GAPDH is being used as a loading control, and the results are from three independent experiments. Additional western blotting data are presented in Figure 4.
Effect of LL-ES of ARVGP on LV function
At baseline, there are no significant differences among the three groups (VERP:P =0.99;LVEDV:P =0.98;LVESV:P =0.95;LVSV:P =0.90;LVEF:P =0.98).VERP increased slightly from 138±6ms in the control group to 139±8ms in the drug group (P =0.85, n=10, Table 1). However, after 1w of LL-ES, VERP significantly increased to 166±13ms compared to the drug group (P =0.001, n=10, Table 1). The LVEDV decreased significantly from 35.39±0.68ml in the control group to 34.20±0.68ml after drug administration (P =0.01, n=10, Table 1),while changed slightly to 34.43±0.66ml after 1 w of LL-ES of ARVGP compared with drug group(P =0.45, n=10, Table 1).Likewise, the LVESV decreased markedly from 22.46±0.51mlin the control group to 21.04±0.54ml after drug administration(P =0.001, n=10, Table 1),and also decreased significantly to 17.57±0.47ml after 1 w of LL-ES of ARVGP compared with drug group(P =0.001, n=10, Table 1).Therefore, the LVSV was calculated as 13.03±0.30ml in the control group and remain nearly constant to 13.16±0.22ml after drug administration(P =0.28, n=10, Table 1) but increased significantly to 16.86±0.27ml after 1 w of LL-ES of ARVGP compared with drug group(P =0.001, n=10, Table 1).As a result, LVEF rising from 36.81±0.66% in the control group to 38.48±0.53%after drug administration (P =0.001, n=10, Table 1). However, after 1 w of LL-ES of ARVGP, the LVEF increased significantly to 48.94±0.57% compared with the drug group (P =0.001, n=10, Table 1).