Fig. 5

Silencing HAPLN1 promoted HF cell viability, reduced apoptosis, and inhibited cardiac hypertrophy and oxidative stress in Ang II-induced AC16 cells (n = 3). (A) The efficiency of HAPLN1 silencing was assessed by RT-qPCR, and sh-HAPLN1-1 exhibited the highest knockdown efficiency. (B) AC16 cell viability was reduced by Ang II treatment and reversed by HAPLN1 silencing as assessed by CCK8. (C) HAPLN1 knockdown reduced apoptosis in Ang II-induced AC16 cells. (D) Western blot illustrated that the protein expressions of cardiomyocyte hypertrophy -associated protein (ANP, BNP, and MMP-1) was reduced after HAPLN1 knockdown in Ang II-induced AC16 cells. (E) Ang II treatment decreased mtDNA content, whereas knockdown of HAPLN1 promoted mtDNA expression as measured by RT-qPCR. (F) ELISA assay showed that mitochondrial ATP generation as well as the activities of complex I and V were decreased in the Ang II group and were increased in the sh- HAPLN1 + Ang II group. (G) HAPLN1 knockdown promoted GSH levels and reduced MDA and ROS levels in the Ang II-induced AC16 cells, which were assessed by ELISA assay The results are presented as the mean ± SD from three independent experiments. ^***P < 0.001 vs. Control group; ^#P < 0.05, ^###P < 0.001 vs. sh-NC + Ang II group. Notes HF, heart failure; RT-qPCR, Real-time reverse transcriptase-polymerase chain reaction; CCK8, cell counting kit-8; ELISA, enzyme-linked immunosorbent assay