Time-Released Black Phosphorus Hydrogel Accelerates Myocardial Repairing through Antioxidant and Motivates Macrophage Polarization Properties.
Jiahui ZhangDi SunYuhan LiaoBingxin CaoRan GaoZhuanglin ZengChuangsheng ZhengYumiao WeiXiaopeng GuoPublished in: Biomaterials research (2024)
The improvement of the myocardial microenvironment largely determines the prognosis of myocardial infarction (MI). After MI, early removal of excessive reactive oxygen species (ROS) in the microenvironment can alleviate oxidative stress injury and promote M2 phenotype polarization of macrophages, which is important for advocating myocardial repair. In this study, we combined traditional natural hydrogel materials chitosan (CS) and gelatin (Gel) to encapsulate polydopamine-modified black phosphorus nanosheets (BP@PDA). We designed an injectable composite gel (CS-Gel-BP@PDA) with a time-released ability to achieve in situ sustained-release BP@PDA in the area of MI. Utilizing the inflammation inhibition ability of CS-Gel itself and the high reactive activity of BP@PDA with ROS, continuous improvement of infarct microenvironment and myocardial repair were achieved. The studies in vivo revealed that, compared with the saline group, CS-Gel-BP@PDA group had alleviated myocardial fibrosis and infarct size and importantly improved cardiac function. Immunofluorescence results showed that the ROS level and inflammatory response in the microenvironment of the CS-Gel-BP@PDA group were decreased. In conclusion, our study demonstrated the time-released ability, antioxidative stress activity and macrophage polarization modulation of the novel composite hydrogel CS-Gel-BP@PDA, which provides inspiration for novel therapeutic modalities for MI.
Keyphrases
- single cell
- hyaluronic acid
- wound healing
- reactive oxygen species
- left ventricular
- oxidative stress
- stem cells
- drug delivery
- dna damage
- inflammatory response
- cell death
- acute myocardial infarction
- tissue engineering
- heart failure
- gold nanoparticles
- weight loss
- toll like receptor
- induced apoptosis
- lipopolysaccharide induced
- acute coronary syndrome
- sewage sludge
- signaling pathway
- quantum dots
- case control
- diabetic rats