scholarly journals Tregs Biomimetic Nanoparticle to Reprogram Inflammatory and Redox Microenvironment in Infarct Tissue to Inhibit the Remodeling of the Left Ventricle of Myocardial Ischemia Reperfusion Injury in Mice

2021 ◽  
Author(s):  
Fangyuan Li ◽  
Daozhou Liu ◽  
Miao Liu ◽  
Qifeng Ji ◽  
Bangle Zhang ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Left Ventricle ◽  
Protein Expression ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Myocardium ◽  
Increased Risk ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Abstract Background At present, patients with myocardial infarction remain an increased risk for myocardial ischemia/reperfusion injury (MI/RI), which currently lacks an effective therapeutic method. It is still a bottleneck that effectively deliver drug to ischemic myocardium to treat MI/RI. Inspired by the protective effect of regulatory T cells (Tregs) on MI/RI and natural role of platelets in adhesion with damaged blood vessel in heart during myocardial infarct, a Tregs biomimetic nanoparticle (CsA@PPTK) was prepared by camouflaging a cyclosporin A (CsA)-loaded and reactive oxygen species (ROS)-sensitive nanoparticle with platelet membrane. Results In MI/RI mice, CsA@PPTK could be preferentially delivered to ischemic myocardium. CsA@PPTK significantly scavenged ROS in ischemic myocardium, while it also markedly increased the generation of Tregs and the ratio of M2 type macrophage to M1 type macrophage in ischemic myocardium. Furthermore, CsA@PPTK significantly attenuated apoptosis of cardiomyocytes in ischemic myocardium. At the same time, CsA@PPTK obviously reduced the infarct size, fibrosis area and the protein expression of MMP-9, while increased the protein expression of CX43. Subsequently, the remodeling of the left ventricle was significant alleviated. Finally, heart function of MI/RI mice was markedly improved. Conclusion CsA@PPTK has great potential in the treatment of MI/RI. This study provides a novel class of heart protective biomimetic platform that is beneficial for treatment of MI/RI.

scholarly journals Total saponins from Trillium Tschonoskii Maxim alleviate myocardial ischemia reperfusion injury in rat

2020 ◽  
Author(s):  
Xiujing Zhang ◽  
Wei Wang ◽  
Jie Tang ◽  
Qin Xie ◽  
Di Ma
Keyword(s):  
Myocardial Ischemia ◽  
Protein Expression ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Pathological Changes ◽  
Apoptosis Protein ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Trillium Tschonoskii

Abstract BackgroundTo investigate the effect and possible mechanisms of total saponins from Trillium Tschonoskii Maxim. (TST) on myocardial ischemia reperfusion injury in rat.Methods and ResultsRats were pre-treated with TST in 100 and 200 mg/kg, respectively. After 14 days intragastric administration, the model of myocardial ischemia-reperfusion injury was established by ligation of the left anterior descending coronary artery for 30 min and then releasing the ligated artery for 120 min. The hemodynamic indexes, anti-oxidation index, and the anti-inflammation factors were detected. Pathological changes in myocardia tissue were observed by H&E staining. Apoptosis protein expression of caspase 3, 9, 12, AMPK, phosphorylation AMPK (p-AMPK) and Sirt1 was detected by Western blot. Pretreating the rats with TST dramatically decreased the levels of MDA, TNF-α, IL-6 and IL-1β, increased the levels of SOD and GSH-Px, and the apoptosis protein expression were all significantly decreased. In addition, the protein expression of p-AMPK and Sirt1 were markedly increased in TST pre-treated group. Furthermore, TST pre-treatment also improved the histopathological changes.ConclusionTST protect the myocardium by reducing the levels of inflammation factors, peroxides and cell apoptosis, increasing the anti-oxidase, and improving the pathological changes. The possible mechanism maybe through the activating of the AMPK/Sirt1 signaling pathway.

scholarly journals Protective anti-inflammatory effect of ADAMTS13 on myocardial ischemia/reperfusion injury in mice

Blood ◽  
2012 ◽  
Vol 120 (26) ◽  
pp. 5217-5223 ◽  
Author(s):  
Simon F. De Meyer ◽  
Alexander S. Savchenko ◽  
Michael S. Haas ◽  
Daphne Schatzberg ◽  
Michael C. Carroll ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Myocardium ◽  
Wild Type ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Anti Inflammatory ◽  
Myocardial Ischemia Reperfusion ◽  
Inflammatory Effect

Abstract Coronary heart disease is a major cause of death in the western world. Although essential for successful recovery, reperfusion of ischemic myocardium is inevitably associated with reperfusion injury. To investigate a potential protective role of ADAMTS13, a protease cleaving von Willebrand factor multimers, during myocardial ischemia/reperfusion, we used a mouse model of acute myocardial infarction. We found that Adamts13−/− mice developed larger myocardial infarctions than wild-type control mice, whereas treatment of wild-type mice with recombinant human ADAMTS13 (rhADAMTS13) led to smaller infarctions. The protective effect of ADAMTS13 was further confirmed by a significant reduction of cardiac troponin-I release and less myocardial apoptosis in mice that received rhADAMTS13 compared with controls. Platelets adherent to the blood vessel wall were observed in few areas in the heart samples from mice treated with vehicle and were not detected in samples from mice treated with rhADAMTS13. However, we observed a 9-fold reduction in number of neutrophils infiltrating ischemic myocardium in mice that were treated with rhADAMTS13, suggesting a potent anti-inflammatory effect of ADAMTS13 during heart injury. Our data show that ADAMTS13 reduces myocardial ischemia/reperfusion injury in mice and indicate that rhADAMTS13 could be of therapeutic value to limit myocardial ischemia/reperfusion injury.

Recent Advance on Drug Therapy Related to Myocardial Ischemia Reperfusion Injury

2022 ◽  
Vol 12 (2) ◽  
pp. 299-305
Author(s):  
Yuezhu Liu ◽  
Hua Zeng ◽  
Junmei Xu
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Pathological Process ◽  
Ischemic Myocardium ◽  
Research Progress ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Artery Obstruction

Myocardial ischemia reperfusion injury (MIRI) means complete or partial artery obstruction of coronary artery, and ischemic myocardium will be recirculating in a period of time. Although the ischemic myocardium can be restored to normal perfusion, its tissue damage will instead be progressive. An aggravated pathological process. MIRI is a complex entity where many inflammatory mediators play different roles, both to enhance myocardial infarction-derived damage and to heal injury. Therefore, the research and development of drugs for the prevention and treatment of this period has also become the focus. This article first studied pathophysiology of MIRI, and reviewed the research progress of MIRI-related drugs. Research results show that: MIRI is inevitable for myocardial ischemia, with the possible to double damage via the ischemic condition. Therefore, it is a serious complication and one of the most popular diseases in the world. It has always been difficult to find an effective treatment for this disease, because it is difficult to explore the inflammation behind its pathophysiology.

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