No abstract

Regulatory T cells overexpressing SPARC (secreted protein acidic and cysteine rich) (Sparc high Tregs) can help repair infarct tissues after acute myocardial infarction (AMI). This research demonstrates thatSparc high Treg-derived extracellular vesicles (EVs) effectively improved cardiac function through proinflammatory factors IL-1𝜷, IL-6, and TNF-𝜶 inhibition and collagen synthesis related gene Col3a1 promotion in AMI; moreover, a composite hydrogel-EVs system (DHPM(4APPC)_EVs) is designed based on Sparc high Treg-derived EVs with CXCR2 overexpressing and pH/H 2 O 2 /MMP9 temporally responsive gel microspheres. In AMI, due to the levels of chemokine, pH, H 2 O 2 , and MMP9 enzymes in the infarct area, DHPM(4APPC)_EVs can effectively target the infarct area, release the loaded EVs, form the gel to capture the released EVs, and slowly release the captured EVs, contribute to promote EVs to stay in the infarct area for a long time to play the repair function, so as to reduce myocardial injury and promote the improvement of cardiac function. The proposed system in this research provides a potential approach for the treatment of AMI in the future.

Rheumatoid arthritis (RA) is a chronic, systemic, and autoimmune disease, and its main pathological changes are inflammatory cell infiltration accompanied by the secretion and accumulation of a variety of related cytokines, which induce the destruction of cartilage and bone tissue. Therefore, the modulation of inflammatory cells and cytokines is a key therapeutic target for controlling inflammation in RA. This review details the effects of emodin on the differentiation and maturation of T lymphocytes, dendritic cells, and regulatory T cells. In addition, the systematic introduction of emodin directly or indirectly affects proinflammatory cytokines (TNF-α, IL-6, IL-1, IL-1β, IL-17, IL-19, and M-CSF) and anti-inflammatory cytokines (the secretion of IL-4, IL-10, IL-13, and TGF-β) through the coregulation of a variety of inflammatory cytokines to inhibit inflammation in RA and promote recovery. Understanding the potential mechanism of emodin in the treatment of RA in detail provides a systematic theoretical basis for the clinical application of emodin in the future.