Effect of Pilose Antler Peptide on Doxorubicin-induced H9c2 Cells Injury via TGF-beta/Smad/ERK Signaling Pathway

Doxorubicin (DOX) is widely used clinically for the treatment of various malignant tumors, but it is accompanied by severe body toxic reactions, especially cardiac toxicity. This article explores the effects of pilose antler peptide (PAP) on DOX-induced myocardial injury and related mechanisms through in vitro experiments. Different concentrations of DOX were used to treat H9c2 cells for 6, 12, 24, and 48 h, respectively, to determine the IC50. Different concentrations of PAP were treated to H9c2 cells for 24, 48, and 72 h to determine the effect of PAP on H9c2 cells. The experiment was divided into control group, DOX group, PAP group and DOX+PAP group. Lactate dehydrogenase (LDH) leakage and creatine kinase MB (CK-MB) level were used to detect cell viability, flow cytometry was used to detect cell cycle and apoptosis, and immunofluorescence was used to detect Bax and Bcl-2 expression. The protein levels of TGF-beta / Smad / ERK signaling pathway were detected by Western blot. We found that PAP significantly increased cell viability after DOX-induced injury, reduced LDH, CK-MB levels, up-regulated Bcl-2 expression and down-regulated Bax expression levels. In addition, PAP can delay cell G2/M phase arrest, reduce apoptosis, significantly reduce TGF-beta(1) protein levels and Smad2, Smad3, ERK phosphorylation levels. These results suggest that PAP can protect DOX-induced H9c2 damage by inhibiting the TGF-beta / Smad / ERK signaling pathway.