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Huimin Bian
Nanjing University of Chinese Medicine
Corresponding Author
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Aim of the study: Salvianolic acid B(Sal B) as a natural compound extracted from Salvia miltiorrhiza, has been extensively used to protect cardiomyocytes from myocardial ischemia. Although Sal B has shown evident effects on cardiovascular diseases, the detailed mechanism is still unclear as yet. Herein, we intended to explorethe protective effects of Sal B on myocardial ischemic injury and the underlying mechanism.
Methods and Results: Western blotting, immunofluorescence assay, flow cytometry and lentiviral transfection were performed. The mice with myocardial ischemic injury were intravenously given 10 mg/kg Sal B once daily for seven days, and then H9c2 cells were treated with Sal B (20, 40, 80 μmol/L). Sal B treatment protected cardiomyocytes from myocardial ischemia through relieving apoptosis. Transmission electron microscopy and fluorescence microscopy exhibited that Sal B significantly increased autophagic lysosomes and vacuoles in H9c2 cells. Administration with Sal B significantly up-regulated the expressions of autophagy-related factors such as LC3, Atg5 and Beclin 1 in H9c2 cells and myocardial tissues. The beneficial autophagic changes induced by Sal B were abrogated through pharmacological inhibition.
Conclusions: This study provides a molecular mechanism by which Sal B potently inhibits apoptosis and oxidative stress upon myocardial ischemia by activating the AMPK-autophagy pathway. Sal B is a potential agent for treating myocardial ischemia.
Keywords
Salvianolic acid B, Myocardial ischemia, Autophagy, Apoptosis, AMPK
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- table1.jpg
Table.1. *P < 0.05, **P < 0.01, ***P < 0.001 vs. Control group; #P < 0.05, ##P < 0.01 vs. Model group, &P < 0.05, &&P < 0.01 vs. Sal B group.
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A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
Huimin Bian
Nanjing University of Chinese Medicine
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 17 Nov, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Internal Medicine
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Aim of the study: Salvianolic acid B(Sal B) as a natural compound extracted from Salvia miltiorrhiza, has been extensively used to protect cardiomyocytes from myocardial ischemia. Although Sal B has shown evident effects on cardiovascular diseases, the detailed mechanism is still unclear as yet. Herein, we intended to explorethe protective effects of Sal B on myocardial ischemic injury and the underlying mechanism.
Methods and Results: Western blotting, immunofluorescence assay, flow cytometry and lentiviral transfection were performed. The mice with myocardial ischemic injury were intravenously given 10 mg/kg Sal B once daily for seven days, and then H9c2 cells were treated with Sal B (20, 40, 80 μmol/L). Sal B treatment protected cardiomyocytes from myocardial ischemia through relieving apoptosis. Transmission electron microscopy and fluorescence microscopy exhibited that Sal B significantly increased autophagic lysosomes and vacuoles in H9c2 cells. Administration with Sal B significantly up-regulated the expressions of autophagy-related factors such as LC3, Atg5 and Beclin 1 in H9c2 cells and myocardial tissues. The beneficial autophagic changes induced by Sal B were abrogated through pharmacological inhibition.
Conclusions: This study provides a molecular mechanism by which Sal B potently inhibits apoptosis and oxidative stress upon myocardial ischemia by activating the AMPK-autophagy pathway. Sal B is a potential agent for treating myocardial ischemia.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
This is a list of supplementary files associated with this preprint. Click to download.
- table1.jpg
Table.1. *P < 0.05, **P < 0.01, ***P < 0.001 vs. Control group; #P < 0.05, ##P < 0.01 vs. Model group, &P < 0.05, &&P < 0.01 vs. Sal B group.
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