After myocardial ischemia/reperfusion injury (MI/RI), endothelial cell injury causes impaired angiogenesis and obstruction of microcirculation, resulting in an inflammatory outburst that exacerbates the damage. Therefore, synergistic blood vessel repair and inflammation inhibition are effective therapeutic strategies. In this study, we developed a platelet membrane (PM)-encapsulated baicalin nanocrystalline (BA NC) nanoplatform with a high drug load, BA NC@PM, which co-target to endothelial cells and macrophages through the transmembrane proteins of the PM to promote angiogenesis and achieve anti-inflammatory effects. In vitro cell scratch assays and transwell assay manifested that BA NC@PM could promote endothelial cell migration, as well as increase mRNA expression of CD31 and VEGF in the heart after treatment of MI/RI mice, suggesting its favorable vascular repair function. In addition, the preparation significantly reduced the expression of pro-inflammatory factors and increased the expression of anti-inflammatory factors in plasma, promoting the polarization of macrophages. Our study highlights a strategy for enhancing the treatment of MI/RI by promoting angiogenesis and regulating macrophage polarization via the biomimetic BA NC@PM nanoplatform.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.colsurfb.2024.114159 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
From smog to scarred hearts: unmasking the detrimental impact of air pollution on myocardial ischemia-reperfusion injury.
Cell Mol Life Sci
January 2025
Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.
Air pollution is a global environmental health hazard associated with elevated cardiovascular morbidity and mortality. Emerging evidence suggests that exposure to various air pollutants, specifically particulate matter (PM), ultrafine particulate matter (UFPM), and diesel exhaust particles, may exacerbate myocardial ischemia-reperfusion (I/R) injury. PM exposure can directly impair cardiomyocyte survival under ischemic conditions by inducing inflammation, oxidative stress, apoptosis, and dysregulation of non-coding RNAs.
View Article and Find Full Text PDFThe Multifaceted Roles of BACH1 in Disease: Implications for Biological Functions and Therapeutic Applications.
Adv Sci (Weinh)
January 2025
Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Department of Rheumatology, Zhongshan Hospital, Zhongshan Hospital Immunotherapy Translational Research Center, Fudan University, Shanghai, 200032, China.
BTB domain and CNC homolog 1 (BACH1) belongs to the family of basic leucine zipper proteins and is expressed in most mammalian tissues. It can regulate its own expression and play a role in transcriptionally activating or inhibiting downstream target genes. It has a crucial role in various biological processes, such as oxidative stress, cell cycle, heme homeostasis, and immune regulation.
View Article and Find Full Text PDFPreconditioning with acteoside ameliorates myocardial ischemia‑reperfusion injury by targeting HSP90AA1 and the PI3K/Akt signaling pathway.
Mol Med Rep
March 2025
Department of Cardiology, The First Affiliated Hospital to Jiamusi University, Jiamusi, Heilongjiang 154000, P.R. China.
The present study aimed to investigate the cardioprotective effects of acteoside (AC) on myocardial ischemia‑reperfusion injury (MIRI). To meet this aim, a network pharmacological analysis was conducted to search for key genes and signaling pathways associated with AC and MIRI. The infarct size of the rat heart was evaluated using 2,3,5‑triphenyltetrazolium chloride staining, and the serum levels of creatine kinase MB isoenzyme, cardiac troponin I, malondialdehyde and superoxide dismutase were subsequently detected in an experiment.
View Article and Find Full Text PDFRemimazolam alleviates myocardial ischemia/reperfusion injury and inflammation via inhibition of the NLRP3/IL‑1β pathway in mice.
Int J Mol Med
April 2025
Department of Anesthesiology, Affiliated Hospital, Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Remimazolam (Rema) is a novel anesthetic that is widely used in anesthesia and sedation in critically ill patients. Notably, Rema exerts effects in patients through activation of the γ‑aminobutyric acid (GABA) receptor. GABA may alleviate myocardial ischemia/reperfusion (I/R) injury; however, the impact of Rema and underlying molecular mechanism in myocardial I/R injury remain to be fully understood.
View Article and Find Full Text PDFThe link between ferroptosis and autophagy in myocardial ischemia/reperfusion injury: new directions for therapy.
J Cardiovasc Transl Res
January 2025
Department of Cardiology, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, China.
Myocardial ischemia/reperfusion (I/R)-induced cell death, such as autophagy and ferroptosis, is a major contributor to cardiac injury. Regulating cell death may be key to mitigating myocardial ischemia/reperfusion injury (MI/RI). Autophagy is a crucial physiological process involving cellular self-digestion and compensation, responsible for degrading excess or malfunctioning long-lived proteins and organelles.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!