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).