3.4 LCZ696 treatment and TLR2 knockdown attenuated
doxorubicin-induced H9C2 cell fibrosis in vitro.
Next, H9C2 cells were cultured to further confirm the potential effect
of LCZ696 treatment and TLR2 deficiency in cardiac injury induced by
DOX, and we then determined the role of TLR2 in DOX treatment.
TLR2 siRNA was used to silence the expression of TLR2 in the H9C2 cell
line (Figure 4A). As expected, DOX stimulated significantly high levels
of collagen I and TGF-β protein and mRNA, which were normalized to the
control levels as the TLR2 was knocked down in H9C2 cells (Figure 4C-F).