Ginsenoside Rg2 protects cardiomyocytes against trastuzumab‑induced toxicity by inducing autophagy
- Guang Liu
- Xiaoyong Qi
- Xingtao Li
- Fangyi Sun
Affiliations: Department of Cardiovascular Medicine, Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China, Department of Cardiovascular Medicine, Hebei General Hospital, Shijiazhuang, Hebei 050000, P.R. China, Department of Cardiovascular Medicine, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China
- Published online on: March 11, 2021 https://doi.org/10.3892/etm.2021.9904
Copyright: © Liu
et al. This is an open access article distributed under the
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Trastuzumab (TZM) significantly improves the outcomes of patients with breast cancer; however, it is associated with severe cardiotoxicity. Ginsenoside Rg2 was reported to exert protective effects against myocardial injury and apoptosis in human cardiomyocytes (HCMs). However, whether ginsenoside Rg2 protects HCMs against TZM‑induced toxicity remains unclear. The present study investigated the proliferation of HCMs using a Cell Counting Kit‑8 assay and Ki67 immunofluorescence staining. Apoptotic cells were detected by Annexin V/propidium iodide staining and flow cytometry. Furthermore, monodansylcadaverine staining was performed to detect cell autophagy. In addition, western blotting was used to detect the expression levels of phosphorylated (p)‑Akt, p‑mTOR, beclin 1, microtubule associated protein 1 light chain 3α (LC3) and autophagy protein 5 (ATG5) in HCMs. Pretreatment with ginsenoside Rg2 significantly protected HCMs against TZM‑induced cytotoxicity by inhibiting apoptosis. Furthermore, pretreatment with ginsenoside Rg2 induced autophagy in HCMs by upregulating the expression levels of p‑Akt, p‑mTOR, beclin 1, LC3 and ATG5. The results obtained in the present study suggested that ginsenoside Rg2 could protect HCMs against TZM‑induced cardiotoxicity by activating autophagy. Therefore, ginsenoside Rg2 may serve as a potential therapeutic agent to prevent TZM‑related cardiotoxicity in patients with breast cancer.