Research Article
Cryptotanshinone Attenuated Pathological Cardiac Remodeling In Vivo and In Vitro Experiments
Figure 5
CTS treatment inhibited AngII induced cardiomyocyte hypertrophy in vitro. (a) CCK-8 was used to determine the cell viability after treating different concentration of CTS (0, 3, 6, 12, and 24 μM) for 48 hours; (b) representative fluorescent pictures for α-actin and NRCMs were treated with AngII (1 μM) or CTS for 48 hours; (c) calculating the CSA according to the fluorescent pictures, about 100 NRCMs were used for calculating; (d) representative Western blots of p-STAT3, T-STAT3, and GAPDH; NRCMs were incubated with AngII or CTS (3, 6, or 12 μM) for 12 h; (e) relative quantification of p-STAT3/T-STAT3 and T-STAT 3; (f) representative Western blots of p-STAT3, T-STAT3, and Histone H3; NRCMs were incubated with AngII or CTS (3, 6, or 12 μM) for 12 h, and then isolate the nucleus proteins from NRCMs for analysis; (g) relative quantification of p-STAT3/T-STAT3 and T-STAT 3; (h) representative Western blots of p-STAT3, T-STAT3, ANP, β-MHC, BNP, and GAPDH; NRCMs were transfected with adenovirus for mediating GFP or STAT3 overexpression during 24 h and then were incubated with CTS or AngII as indicated in picture for another 12 hours before collecting for total protein extraction; (i) relative quantification of p-STAT3/T-STAT3, T-STAT3, ANP, β-MHC, and BNP; all phosphorylated proteins were normalized to corresponding total protein and then normalized to GAPDH before relative quantification; cell experiments were repeated three times independently. Compared with the PBS-treated group (); #compared with the AngII-treated group ().
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