The hypoxia microenvironment of solid tumors poses a technological bottleneck for ferroptosis and immunotherapy in clinical oncology. Nanoreactors based on special physiological signals in tumor cells are able to avoid various tumor tolerance mechanisms by alleviating the intracellular hypoxia environment. Herein we reported a nanoreactor Cu 2−x Se that enabled the conversion of Cu elements between Cu + and Cu 2+ for the generation of O 2 and the consumption of intracellular GSH content. Furthermore, to enhance the catalytic and ferroptosis-inducing activities of the nanoreactors, the ferroptosis agonist Erastin was loaded on the ZIF-8 coating on the surface of Cu 2−x Se to up-regulate the expression of NOX4 protein, increase the intracellular H 2 O 2 content, catalyze the Cu + to produce O 2 and activate ferroptosis. In addition, the nanoreactors were simultaneously surface functionalized with PEG polymer and folic acid molecules, which ensured the in vivo blood circulation and tumor-specific uptake. In vitro and in vivo experiments demonstrated that the functionalized self-supplying nanoreactors can amplify the ability to generate O 2 and consume intracellular GSH via the interconversion of Cu elements Cu + and Cu 2+ , and impair the GPX4/GSH pathway and HIF-1α protein expression. At the same time, by alleviating the intracellular hypoxia environment, the expression of miR301, a gene in the secreted exosomes was decreased, which ultimately affected the phenotype polarization of TAMs and increased the content of IFN γ secreted by CD8 + T cells, which further promoted the ferroptosis induced by Erastin-loaded nanoreactors. This combined therapeutic strategy of activating the tumor immune response and ferroptosis via self-supplying nanoreactors provides a potential strategy for clinical application.

The retention of fat-derived grafts remains a challenge for regenerative medicine. Fat aspirates from patients undergoing liposuction were prepared into standard Coleman fat grafts or further isolated using mechanical shear force to prepare a stromal vascular fraction (SVF)/extracellular matrix (ECM) gel. The retention rate of the SVF/ECM gel was significantly higher than that of the Coleman fat at 3, 14, 28, and 60 days following transplantation on the backs of nude mice. The viscosity of the fat was directly proportional to the shearing force. Although the mechanical isolation did not affect the total number of cells, it significantly decreased the number of living cells. Flow cytometry showed a greater number of mesenchymal stem cells, supra-adventitial (SA)-adipose stromal cells (ASCs), and adipose-derived stem cells but a lower number of endothelial progenitor cells in the SVF/ECM gel than in the Coleman fat. Thus, mechanical isolation of fat can increase the pluripotency of adipocytes, which can improve graft retention in cell therapy.

Androgenetic alopecia (AGA) is a hair loss disease. At present, use of the stromal vascular fraction (SVF) and platelet-rich plasma (PRP) are thought to be the novel, safe, and effective treatment options of AGA, but the mechanism by which SVF and PRP promote hair growth is unclear. Here, we investigated the mechanism underlying the effects of SVF and PRP on hair growth by in vitro culture and in vivo modeling. SVF and PRP promoted hair growth, as was evident from the observation and counting of hair on the back skin of nude mice using ImageJ software. SVF and PRP promoted hair growth, and SVF worked better. We performed nucleic acid extraction with nanomagnetic beads, and the protein levels were extracted with a bicinchoninic acid protein assay kit. The results of western blot analysis and quantitative polymerase chain reaction (qPCR) showed that both SVF and PRP promoted the expression of anti-apoptotic genes. The effect of SVF was better than that of PRP. The results of EdU and hematoxylin and eosin staining showed that SVF and PRP induced the proliferation of hair follicle cells. SVF exerted better effects on the proliferation of hair follicle cells than PRP. Enzyme-linked immunosorbent assay (ELISA) results showed that the expression of the proteins associated with the Wnt/β-catenin process, including vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), alkaline phosphatase (ALP), Wnt10b, and β-catenin, significantly increased in the SVF-treated and PRP-treated dermal/epidermal cells as compared with the control cells. Therefore, SVF and PRP increased the expression of VEGF and PDGF through the Wnt/β-catenin signaling pathway to promote hair growth. The effect of SVF on dermal cells/epidermal cells was stronger than that of PRP, and the difference was statistically significant (P < 0.05).

Acne was treated by combining the N-terminal of HPA3NT3 (where Lys in position 13 was replaced by Asn) and the C-terminal antibacterial peptide HAG of GLP-1 (32–36) amide pentapeptide after amino replacement. The minimal inhibitory concentration (MIC) was measured using the broth dilution method to evaluate HAG’s antibacterial activity. HAG’s cytotoxicity was determined using water-soluble tetrazolium salt (WST-1). Interleukin-8 (IL-8) expression in human immortalized keratinocytes (HaCaT) cells stimulated by Propionibacterium acnes and treated with HAG was measured by Enzyme-linked immunosorbent assay (ELISA). IL-8 and toll-like receptor 2 (TLR2) expression was detected using real-time reverse transcriptase polymerase chain reaction (qRTPCR) to analyze HAG’s anti-inflammatory effect in vitro. The total RNA was extracted using SiO2 nanoparticles. Oil red O staining was used to detect the intracellular lipid drop of Sebaceous Gland Cell Line (SZ95), and ELISA was used to detect triglyceride levels. Hematoxylin-eosin (HE) staining was used to evaluate ear edema induced by Propionibacterium acne in mice. The MIC of HAG in Propionibacterium acnes was 6.3 μg/mL, and 50 μg/mL of HAG showed cytotoxicity. HAG significantly reduced TLR2 and IL-8 expression in HaCaT cells. Oil red O staining showed that the lipid distribution of HAG-treated SZ95 and triglyceride secretion decreased. HAG reduced ear swelling induced by Propionibacterium acnes. HAG has anti-bacterial and anti-inflammatory effects, excellent hypolipidemic function, and low cytotoxicity. Further development of HAG could be a promising and effective reagent for acne therapy.

We used intervention means to investigate the mechanism of LncRNA-ATB involved in the development and progression of Scleroderma by examining the expression differences of LncRNA-ATB between lesional skin of Scleroderma patients and normal skin using a cellular model. Lesional skin and normal skin recruited from five patients with Scleroderma diagnosed in the outpatient clinic were designed as experimental and control groups respectively, established a fibroblast cell model. (1) Magnetic nanoparticles aided in the quantitative determination of LncRNA-ATB in tissue and fibroblasts respectively; (2) Determine the level of transcription and protein expression of fibrosis-related genes before and after Scleromderma Group interference. LncRNA-ATB regulates fibrotic mechanisms in Scleroderma by influencing collagen and fibronectin transcriptional synthesis in Scleroderma fibroblasts.