Propofol and salvianolic acid A synergistically attenuated cardiac ischemia–reperfusion injury in diabetic mice via modulating the CD36/AMPK pathway
- Burns & Trauma Vol. 12, Issue 1, (2024)
- 作者机构：
1. Department of Anesthesiology, Affiliated Hospital of Guangdong Medical University
2. State Key Laboratory of Pharmaceutical Biotechnology
3. The University of Hong Kong
4. Department of Orthopaedics and Traumatology, The University of Hong Kong
5. Department of Anesthesiology, The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University
6. Department of Health Technology and Informatics, The Hong Kong Polytechnic University, No. 11 Yucai Road, hung hom, Kowloon,Hong Kong
7. Spinal Division of Orthopedic and Traumatology Center, The Affiliated Hospital of Guangdong Medical University
8. Faculty of Chinese Medicine
9. Macau University of Science and Technology
- 作者简介：
- 基金信息：
DOI：10.1093/burnst/tkad055
CLC：Published：2024，
Published Online：9 April 2024，
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Jiaqi Zhou, Weiyi Xia, Jiajia Chen, Kaijia Han, Yuxin Jiang, Anyuan Zhang, Dongcheng Zhou, Danyong Liu, Jiefu Lin, Yin Cai, Guanghua Chen, Liangqing Zhang, Aimin Xu, Youhua Xu, Ronghui Han, Zhengyuan Xia, Propofol and salvianolic acid A synergistically attenuated cardiac ischemia–reperfusion injury in diabetic mice via modulating the CD36/AMPK pathway, Burns & Trauma, Volume 12, 2024, tkad055, https://doi.org/10.1093/burnst/tkad055
Jiaqi Zhou, Weiyi Xia, Jiajia Chen, Kaijia Han, Yuxin Jiang, Anyuan Zhang, Dongcheng Zhou, Danyong Liu, Jiefu Lin, Yin Cai, Guanghua Chen, Liangqing Zhang, Aimin Xu, Youhua Xu, Ronghui Han, Zhengyuan Xia, Propofol and salvianolic acid A synergistically attenuated cardiac ischemia–reperfusion injury in diabetic mice via modulating the CD36/AMPK pathway, Burns & Trauma, Volume 12, 2024, tkad055, https://doi.org/10.1093/burnst/tkad055 DOI：
摘要
Abstract
BackgroundPrevention of diabetic heart myocardial ischemia–reperfusion (IR) injury (MIRI) is challenging. Propofol attenuates MIRI through its reactive oxygen species scavenging property at high doses
while its use at high doses causes hemodynamic instability. Salvianolic acid A (SAA) is a potent antioxidant that confers protection against MIRI. Both propofol and SAA affect metabolic profiles through regulating Adenosine 5‘-monophosphate-activated protein kinase (AMPK). The aim of this study was to investigate the protective effects and underlying mechanisms of low doses of propofol combined with SAA against diabetic MIRI.MethodsDiabetes was induced in mice by a high-fat diet followed by streptozotocin injection
and MIRI was induced by coronary artery occlusion and reperfusion. Mice were treated with propofol at 46 mg/kg/h without or with SAA at 10 mg/kg/h during IR. Cardiac origin H9c2 cells were exposed to high glucose (HG) and palmitic acid (PAL) for 24 h in the absence or presence of cluster of differentiation 36 (CD36) overexpression or AMPK gene knockdown
followed by hypoxia/reoxygenation (HR) for 6 and 12 h.ResultsDiabetes-exacerbated MIRI is evidenced as significant increases in post-ischemic infarction with reductions in phosphorylated (p)-AMPK and increases in CD36 and ferroptosis. Propofol moderately yet significantly attenuated all the abovementioned changes
while propofol plus SAA conferred superior protection against MIRI to that of propofol. In vitro
exposure of H9c2 cells under HG and PAL decreased cell viability and increased oxidative stress that was concomitant with increased levels of ferroptosis and a significant increase in CD36
while p-AMPK was significantly reduced. Co-administration of low concentrations of propofol and SAA at 12.5 μM in H9c2 cells significantly reduced oxidative stress
ferroptosis and CD36 expression
while increasing p-AMPK compared to the effects of propofol at 25 μM. Moreover
either CD36 overexpression or AMPK silence significantly exacerbated HR-induced cellular injuries and ferroptosis
and canceled propofol- and SAA-mediated protection. Notably
p-AMPK expression was downregulated after CD36 overexpression
while AMPK knockdown did not affect CD36 expression.ConclusionsCombinational usage of propofol and SAA confers superior cellular protective effects to the use of high-dose propofol alone
and it does so through inhibiting HR-induced CD36 overexpression to upregulate p-AMPK.
关键词
Keywords
Diabetic cardiomyopathyMyocardial ischemia–reperfusionSalvianolic acid AAMPKCD36PropofoldiabetesPalmitic acid
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