Objective  To explore the mechanism of Qiliqiangxin protecting the cardiomyocytes against oxidative stress.

Methods  H9C2 cells were exposed to hydrogen peroxide (H₂O₂) to establish an oxidative stress-induced injury model and were divided into four groups: control group, H₂O₂ injury group, Qiliqiangxin rescue group (post-injury), and Qiliqiangxin prevention group (pre-treatment). Cell viability was assessed using cell counting Kit-8 (CCK-8) assay. Apoptosis rates were measured by flow cytometry. The expression of miR-21-5p was quantified using RT-qPCR. The levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), phosphatase and tensin homolog (PTEN), phosphoinositide 3-kinase (PI3K), protein kinase B (Akt), and phosphorylated Akt (p-Akt) were evaluated by Western blot analysis.

Results H₂O₂ significantly reduced cell viability and increased apoptosis of H9C2 cells (P＜0.05). No statistically significant difference was observed in the Qiliqiangxin rescue group. However, Qiliqiangxin pre-treatment markedly enhanced cell viability and reduced apoptotic rates compared with the H₂O₂ injury group (P＜0.05). These protective effects were associated with downregulation of PTEN and upregulation of Bcl-2/Bax ratio, miR-21-5p, PI3K, and p-Akt/Akt ratio.

Conclusions  Qiliqiangxin can protect H9C2 cells against oxidative stress-induced injury, which may be associated with regulation of miR-21-5p/PTEN/PI3K/Akt signaling pathway.