医学
心肌梗塞
体内
移植
马森三色染色
标记法
内科学
心脏病学
巨噬细胞
流式细胞术
纤维化
细胞凋亡
心脏纤维化
免疫学
化学
免疫组织化学
体外
生物
生物技术
生物化学
作者
Rundu Chen,Ying-Qian Zhang,Hao Zhou,Yingyun Hu,Yundai Chen
出处
期刊:Journal of Cardiovascular Pharmacology
[Ovid Technologies (Wolters Kluwer)]
日期:2023-10-01
卷期号:82 (4): 287-297
被引量:3
标识
DOI:10.1097/fjc.0000000000001466
摘要
Abstract: Macrophages play an important role in the progression of acute myocardial infarction (AMI). Studies have shown that sodium-dependent glucose transporter 2 inhibitor (SGLT2i) after AMI could increase the proportion of M2 type/M1 macrophages and reduces adverse ventricular remodeling (AVR) post-AMI. This study aimed to investigate whether SGLT2i-pretreated macrophage transplantation could reduce AVR after AMI and the underlying mechanisms. C57BL/6 mice were used to establish an AMI model by ligating the coronary arteries. Dynamic observation of transplanted bone marrow-derived macrophages (BMDMs) was performed using an in vivo imaging system. Cardiac function was assessed using echocardiography. The fibrosis ratio was measured using Masson's trichrome staining. Cardiomyocyte (CM) apoptosis was measured using the TUNEL assay. Macrophage subtypes were measured using flow cytometry. We detected the expression of inflammatory factors in the myocardium and serum using enzyme-linked immunosorbent assay and reverse transcription-polymerase chain reaction. The in vivo imaging system revealed that transplanted SGLT2i-pretreated BMDMs were present in the infarcted myocardium for 7 days. Flow cytometry revealed that SGLT2i-pretreated BMDMs promoted the conversion of native-derived macrophages to the M2 type. SGLT2i-pretreated BMDMs also reduced inflammatory factors (IL-6, TNFα, and IL-1β) in the infarcted myocardium and serum. At 28 days post-AMI, SGLT2i-pretreated BMDMs increased cardiac function and vascular density, but reduced CM hypertrophy. SGLT2i-pretreated BMDMs could reduce CM apoptosis and fibrotic area ratio. In conclusion, transplanted SGLT2i-pretreated BMDMs were present in the infarcted myocardium for 7 days and improved AVR by reducing inflammation and modulating the conversion of native mice-derived macrophages to M2-type macrophages.
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