Research Paper Volume 15, Issue 21 pp 12400—12412
Shenmai injection ameliorates doxorubicin-induced myocardial injury by suppressing autophagy-apoptosis via miR-30a
- 1 Department of Integrated Traditional and Western Medicine, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China
- 2 National Clinical Research Center for Cancer, Tianjin 300060, China
- 3 Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China
- 4 Tianjin’s Clinical Research Center for Cancer, Tianjin 300060, China
- 5 First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300381, China
- 6 National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin 300381, China
Received: June 26, 2023 Accepted: October 12, 2023 Published: November 7, 2023
https://doi.org/10.18632/aging.205188How to Cite
Copyright: © 2023 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Context: Autophagy-apoptosis is the core mechanism of doxorubicin-induced myocardial injury. miR-30a is a pivotal factor in the regulation of autophagy and apoptosis. It remains unclear whether SMI exerts cardioprotective effect by regulating autophagy and apoptosis via miR-30a.
Objective: This study evaluates the effects of SMI on ameliorating doxorubicin-induced myocardial injury.
Materials and Methods: The level of LDH and CK, and the expression of miR-30a was detected. mCherry-EGFP-LC3B double fluorescence was used to observe autophagy flow. Apoptosis was detected by Annexin V/PI staining. Western Blot was used to estimate the expression of autophagy related proteins and apoptosis-related proteins.
Results: Compared with the control group, there were evidently decreased cell viability, elevated level of LDH and CK, down-regulated expression of miR-30a in the model group. Data from Western blot and fluorescence indicated that doxorubicin contributed to the elevated autophagy and apoptosis. Compared with the model group, there were increased cell viability, decreased level of LDH and CK, and up-regulated expression of miR-30a in the Shenmai group and the Shenmai + miR-30a inhibitor group. Meanwhile, the results manifested that there were suppressed autophagy flow accompanied by the down-regulated expression of Beclin-1, LC3-II, LC3-II/LC3-I and up-regulated expression of p62 protein, and declined apoptosis rate accompanied by the up-regulated Bcl2 expression and the down-regulated expression of Bax, Cleaved Caspase-9, Cleaved Caspase-9/Caspase-9, Cleaved Caspase-3, Cleaved Caspase-3/Caspase-3 in the Shenmai group and the Shenmai + miR-30a inhibitor group.
Discussion and Conclusion: Shenmai injection inhibited autophagy and apoptosis via miR-30a, thereby alleviating doxorubicin-induced myocardial injury.