Protective effect of Yiqi Fumai Lyophilized Injection on myocardial cell injury induced by doxorubicin and its mechanism
10.3760/cma.j.cn121382-20240509-00401
- VernacularTitle:注射用益气复脉（冻干）对阿霉素诱导的心肌细胞损伤的保护作用及其机制
- Author:
Yanping SHI
1
;
Xiaoying ZHOU
;
Xiangbo GOU
Author Information
1. 天津理工大学化学化工学院，天津 300384
- Keywords:
Doxorubicin;
Myocardial injury;
Yiqi Fumai Lyophilized Injection;
Phosphoinositide 3-kinase;
Protein kinase B
- From:
International Journal of Biomedical Engineering
2024;47(4):305-311
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the protective effect of Yiqi Fumai Lyophilized Injection (YQFM) on myocardial cell injury induced by doxorubicin and its mechanism.Methods:H9c2 cells were divided into the control group, the doxorubicin group, and the YQFM group. Cells in the control group were given routine incubated. H9c2 cells in the doxorubicin group were given doxorubicin (1 μmol/L) and incubated for 24 h. Cells in the YQFM group were given doxorubicin (1 μmol/L) and YQFM (1.5 mg/L) and incubated for 24 h. The cell viability, cell surface area, atrial natriuretic peptide, and brain natriuretic peptide protein expression levels were detected in each group. The levels of oxidative stress factors, including superoxide dismutase (SOD), malondialdehyde, glutathione peroxidase (GSH-Px) and catalase (CAT) were detected in each group. The apoptosis level, mitochondrial membrane potential, apoptotic associated protein such as B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), and c-cysteinyl aspartate specific proteinase-3 (c-Caspase-3), p53 and protein expression level of phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling pathway were detected in each group.Results:YQFM increased the viability ( P < 0.01), decreased the cell surface area ( P < 0.001), and the levels of atrial natriuretic peptide and brain natriuretic peptide proteins ( P < 0.05) of H9c2 cell in the doxorubicin group. In addition, the SOD, GSH-Px, and CAT levels in the YQFM group were higher than those in the doxorubicin group ( P < 0.05, 0.01), while the malondialdehyde level in the YQFM group was lower than that in the doxorubicin group ( P < 0.05). YQFM also reduced the apoptosis level of H9c2 cell in the doxorubicin group ( P < 0.01), increased the level of mitochondrial membrane potential ( P < 0.01) and the Bcl-2/Bax protein expression level ( P < 0.05), and decreased c-Caspase-3 and p53 protein expression levels ( P < 0.05). It was further found that the p-PI3K and p-Akt protein expression levels in the YQFM group were higher than those in the doxorubicin group ( P < 0.05, 0.01). Conclusions:YQFM can inhibit myocardial cell injury induced by doxorubicin, and its mechanism may be related to the inhibition of oxidative stress and activation of PI3K/Akt pathway.
