Bioglass promotes wound healing by inhibiting endothelial cell pyroptosis through regulation of the connexin 43/reactive oxygen species (ROS) signaling pathway.

Bioactive glass (BG) has recently shown great promise in soft tissue repair, especially in wound healing; however, the underlying mechanism remains unclear. Pyroptosis is a novel type of programmed cell death that is involved in various traumatic injury diseases. Here, we hypothesized that BG may promote wound healing through suppression of pyroptosis. To test this scenario, we investigated the possible effect of BG on pyroptosis in wound healing both in vivo and in vitro. This study showed that BG can accelerate wound closure, granulation formation, collagen deposition, and angiogenesis. Moreover, western blot analysis and immunofluorescence staining revealed that BG inhibited the expression of pyroptosis-related proteins in vivo and in vitro. In addition, while BG regulated the expression of connexin43 (Cx43), it inhibited reactive oxygen species (ROS) production. Cx43 activation and inhibition experiments further indicate that BG inhibited pyroptosis in endothelial cells by decreasing Cx43 expression and ROS levels. Taken together, these studies suggest that BG promotes wound healing by inhibiting pyroptosis via Cx43/ROS signaling pathway.

Amino-functionalized cellulose composite for efficient simultaneous adsorption of tetracycline and copper ions: Performance, mechanism and DFT study.

A novel cellulose composite (denoted as PEI@MMA-1) with porous interconnected structure was prepared by adsorbing methyl cellulose (MC) onto microcrystalline cellulose (MCC) and cross-linking polyethyleneimine (PEI) with MCC by the action of epichlorohydrin, which had the excellent adsorption property, wettability and elasticity. The performances of PEI@MMA-1 composite for removing tetracycline (TC), Cu2+ and coexistent pollutant (TC and Cu2+ mixture) were systematically explored. For single TC or Cu2+ contaminant, the maximum adsorption capacities were 75.53 and 562.23 mg/g at 30 °C, respectively, while in the dual contaminant system, they would form complexes and Cu2+ could play a "bridge" role to remarkably promote the adsorption of TC with the maximum adsorption capacities of 281.66 and 253.58 mg/g for TC and Cu2+. In addition, the adsorption kinetics, isotherms and adsorption mechanisms of single-pollutant and dual-pollutant systems have been thoroughly investigated. Theoretical calculations indicated that the amide group of TC molecule with the assistance of Cu2+ interacted with the hydroxyl group of PEI@MMA-1 composite to enhance the TC adsorption capacity. Cycle regeneration and fixed bed column experiments revealed that the PEI@MMA-1 possessed the excellent stability and utility. Current PEI@MMA-1 cellulose composite exhibited a promising application for remediation of heavy metals and antibiotics coexistence wastewater.

Topical Application of Fibroblast Growth Factor 10-PLGA Microsphere Accelerates Wound Healing via Inhibition of ER Stress.

There is a high incidence of acute and chronic skin defects caused by various reasons in clinically practice. The repair and functional reconstruction of skin defects have become a major clinical problem, which needs to be solved urgently. Previous studies have shown that fibroblast growth factor 10 (FGF10) plays a functional role in promoting the proliferation, migration, and differentiation of epithelial cells. However, little is known about the effect of FGF10 on the recovery process after skin damage. In this study, we found that the expression of endogenous FGF10 was increased during wound healing. We prepared FGF10-loaded poly(lactic-co-glycolic acid) (FGF10-PLGA) microspheres, and it could sustain release of FGF10 both in vitro and in vivo, accelerating wound healing. Further analysis revealed that compared with FGF10 alone, FGF10-PLGA microspheres significantly improved granulation formation, collagen synthesis, cell proliferation, and blood vessel density. In the meantime, we found that FGF10-PLGA microspheres inhibited the expression of endoplasmic reticulum (ER) stress markers. Notably, activating ER stress with tunicamycin (TM) reduced therapeutic effects of FGF10-PLGA microspheres in wound healing, whereas inhibition of ER stress with 4-phenyl butyric acid (4-PBA) improved the function of FGF10-PLGA microspheres. Taken together, this study indicates that FGF10-PLGA microspheres accelerate wound healing presumably through modulating ER stress.