Accelerates Skin Wound Healing Research Articles

Fabrication and evaluation of the regenerative effect of a polycaprolactone/chitosan nanofibrous scaffold containing bentonite nanoparticles in a rat model of deep second-degree burn injury.

In the present study, we evaluated the effect of a nanofibrous scaffold including polycaprolactone (PCL), chitosan (CHT), and bentonite nanoparticles (Ben-NPS) on wound healing in order to introduce a novel dressing for burn wounds. PCL, PCL/CHT, and PCL/CHT/Ben-NPS nanofibrous scaffolds were fabricated by the electrospinning technique. Their structural and physiochemical characteristics were investigated by Fourier-transform infrared spectroscopy (FTIR) analysis, scanning electron microscopy (SEM), tensile strength, water contact angle, as well as, swelling and degradation profiles test. The disc diffusion assay was carried out to investigate the antibacterial potential of the scaffolds. In addition, the cell viability and proliferation ability of human dermal fibroblasts (HDFs) on the scaffolds were assessed using MTT assay as well as SEM imaging. The wound-healing property of the nanofibrous scaffolds was evaluated by histopathological investigations during 3,7, and 14 days in a rat model of burn wounds. SEM showed that all scaffolds had three-dimensional, beadles-integrated structures. Adding Ben-NPS into the PCL/CHT polymeric composite significantly enhanced the mechanical, swelling, and antibacterial properties. HDFs had the most cell viability and proliferation values on the PCL/CHT/Ben-NPS scaffold. Histopathological evaluation in the rat model revealed that dressing animal wounds with the PCL/CHT/Ben-NPS scaffold promotes wound healing. The PCL/CHT/Ben-NPS scaffold has promising regenerative properties for accelerating skin wound healing.

Revitalizing Skin Repair: Unveiling the Healing Power of Livisin, a Natural Peptide Calcium Mimetic.

When the skin is damaged, accelerating the repair of skin trauma and promoting the recovery of tissue function are crucial considerations in clinical treatment. Previously, we isolated and identified an active peptide (livisin) from the skin secretion of the frog Odorrana livida. Livisin exhibited strong protease inhibitory activity, water solubility, and stability, yet its wound-healing properties have not yet been studied. In this study, we assessed the impact of livisin on wound healing and investigated the underlying mechanism contributing to its effect. Our findings revealed livisin effectively stimulated the migration of keratinocytes, with the underlying mechanisms involved the activation of CaSR as a peptide calcium mimetic. This activation resulted in the stimulation of the CaSR/E-cadherin/EGFR/ERK signaling pathways. Moreover, the therapeutic effects of livisin were partially reduced by blocking the CaSR/E-cadherin/EGFR/ERK signaling pathway. The interaction between livisin and CaSR was further investigated by molecular docking. Additionally, studies using a mouse full-thickness wound model demonstrated livisin could accelerate skin wound healing by promoting re-epithelialization and collagen deposition. In conclusion, our study provides experimental evidence supporting the use of livisin in skin wound healing, highlighting its potential as an effective therapeutic option.

Biomedical Potential of Keratin-Biphalin Wound Dressing in Diabetic Mice: In Vitro and In Vivo Studies

ABSTRACTStrategies for successful healing of diabetic wounds are lacking. Natural-derived dressings have gained much attention due to their promising properties. We hypothesized that keratin-biphalin fiber-dressing accelerates skin wound healing in a mouse model of diabetes. Keratin fibers were obtained from mouse fur and soaked in a biphalin solution. Studies on NIH/3T3 cells showed that keratin-biphalin fibers increase cell viability. In vivo studies were made on C57BL/6J mice with iatrogenically induced diabetes. Two full-thickness wounds were created on the back of the mice, one untreated and the other treated with an experimental dressing. Western blot analysis, histopathological and immunohistochemical staining were performed. Biphalin was slowly released from keratin fibers. The obtained keratin-biphalin fibers were biocompatible and supported cell growth. Western blot analysis showed that cells treated with our dressing had an increasing expression level of mTOR, and p-AKT 72 h post-treatment compared to 24 h and 48 h. Animal studies showed that the keratin-biphalin dressing accelerated wound healing on days 5 and 15. Treated wounds showed faster reepithelization and developed thicker epidermis. Histopathological and immunohistochemical studies confirmed that keratin-biphalin fibers stimulate macrophage infiltration, which promotes tissue remodeling and regeneration. Exogenous keratin-biphalin fibers p-AKT/mTOR expression protein in vitro and accelerate skin wound healing in diabetic mice.

A Comprehensive Review on Platelet-Rich Plasma Activation: A Key Player in Accelerating Skin Wound Healing.

Platelet-rich plasma (PRP) activation is emerging as a promising and multifaceted tool for accelerating skin wound healing. This review extensively examines PRP's role in wound healing, focusing on its composition, mechanisms of action, activation methods, and clinical applications. PRP's potential to enhance both chronic and acute wound healing and its applications in cosmetic and aesthetic procedures are explored. Furthermore, this review investigates safety concerns, including adverse reactions, infection risks, and long-term safety implications. Looking to the future, emerging technologies, combination therapies, personalized medicine approaches, and regulatory developments are discussed, pointing towards an important and transformative era in wound healing and regenerative medicine. With its wide-ranging implications for healthcare, PRP activation has the potential to become a ubiquitous and essential therapeutic option, improving patient outcomes and reducing healthcare costs.

Simvastatin-Releasing Nanofibrous Peptide Hydrogels for Accelerated Healing of Diabetic Wounds.

Wound healing is one of the major global health concerns in diabetic patients. Simvastatin (SMV) is a poorly soluble oral cholesterol-lowering drug that may aid diabetic wound healing. In the current study, a thixotropic peptide hydrogel of Fmoc-diphenylalanine (FmocFF) containing SMV was designed to accelerate skin wound healing effectively and safely in diabetic mice. FmocFF hydrogels were prepared at various concentrations by using the solvent-triggering technique and characterized by spectroscopic methods such as attenuated total reflection Fourier transform infrared (FT-IR) spectroscopy and fluorimetry. Mechanical behaviors were explored by oscillatory rheology. In model mice, the regenerative potential of the FmocFF-SMV hydrogel was evaluated in terms of wound contraction and closure, tissue regeneration, acute and chronic inflammation, granulation, and re-epithelization. The results showed that FmocFF-SMV hydrogels had an entangled nanofibrous microstructure and shear-thinning characteristics. FmocFF-SMV demonstrated a sustained drug release over 7 days. Compared to the unloaded FmocFF hydrogel, treatment with FmocFF-SMV led to superior diabetic wound recovery and reduced inflammation. Therefore, the utilization of the sustained-release FmocFF-SMV hydrogel formulation could become an attractive choice for topical wound therapy in diabetes patients.

Paeonol accelerates skin wound healing by regulating macrophage polarization and inflammation in diabetic rats.

Diabetic ulcer is usually seen in people with uncontrolled blood sugar. Reportedly, many factors such as impaired glucose metabolism, and macrovascular and microvascular diseases caused angiogenesis disorders and delayed the healing of diabetic ulcers, thus affecting the body's metabolism, nutrition, and immune function. This study aimed to explore the effect of paeonol on skin wound healing in diabetic rats and the related mechanism. A rat model of diabetic ulcer was established. High glucose-treated mouse skin fibroblasts were co-cultured with M1 or M2-polarized macrophages treated with or without paeonol. H&E and Masson staining were used to reveal inflammatory cell infiltration and collagen deposition, respectively. Immunohistochemistry visualized the expression of Ki67, CD31, and vascular endothelial growth factor (VEGF). Western blot was used to detect interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-4, IL-10, CD31, VEGFA, and collagen I/III. The expression of iNOS and arginase 1 was revealed by immunofluorescence staining. Paeonol treatment augmented collagen deposition and the expression of Ki67, CD31, VEGF, and macrophage M2 polarization markers (IL-4 and IL-10) and reduced wound area, inflammatory cell infiltration, and macrophage M1 polarization markers (IL-1β and TNF-α) in the ulcerated area. In vitro, paeonol treatment promoted M2-polarization and repressed M1-polarization in macrophages, thereby improving the repair of cell damage induced by high glucose. Paeonol accelerates the healing of diabetic ulcers by promoting M2 macrophage polarization and inhibiting M1 macrophage polarization.

LB1795 Dual LSD1/HDAC inhibition accelerates skin wound healing

LB1795 Dual LSD1/HDAC inhibition accelerates skin wound healing

Inhibition of CK2α accelerates skin wound healing by promoting endothelial cell proliferation through the Hedgehog signaling pathway.

Diabetes is a chronic disease characterized by perturbed glucose and lipid metabolism, resulting in high blood glucose levels. Many complications induced by endothelial dysfunction can cause disability and even death of diabetic patients. Here, we found that the protein level of casein kinase 2α (CK2α) was increased in the endothelium of mice with type I diabetes (T1D) induced by streptozotocin (STZ) injection. Although a potential correlation between the protein level of CK2α and endothelial dysfunction in diabetes was established, the contribution of CK2α to the progression of endothelial dysfunction in diabetes remained largely unknown. By using CX4945 (a selective CK2α antagonist) and Si-csnk2a1 (small interfering RNA targeting CK2α), we found that inhibition of CK2α accelerated skin wound healing in T1D mice by promoting proliferation of endothelial cells. Administration of CX4945 or Si-csnk2a1 rescued the impaired Hedgehog signaling pathway in high glucose-treated human umbilical vein endothelial cells (HUVECs). Exploration of the underlying molecular mechanism revealed that the protective effect of CK2α inhibition on angiogenesis, which contributes to skin wound healing in diabetic mice, was blocked by administration of GANT61 (an inhibitor targeting the Hedgehog signaling pathway). Our findings establish CK2α as a regulator of endothelial dysfunction in diabetes and demonstrate that inhibition of CK2α accelerates skin wound healing in T1D mice by promoting endothelial cell proliferation via the Hedgehog signaling pathway.

Egg white-derived peptide KPHAEVVLR promotes wound healing in rat palatal mucosa via PI3K/AKT/mTOR pathway

KPHAEVVLR (KR-9) is a peptide derived from egg white hydrolyzed, which has been found to accelerate skin wound healing in mice. However, the effect of KR-9 on wound healing on palatal mucosa in rats remains unknown, and the mechanism through which KR-9 promotes wound healing should be further explored. Herein, we aimed to investigate the effect and mechanism of KR-9 peptide on palatal mucosa wound healing. Our results showed that KR-9 reduced the wound area of palatal mucosa in rats and promoted human gingival fibroblasts(HGFs) migration and proliferation.The peptide can enter into cytoplasm. It also increased the phosphorylation of PI3K, AKT, and mTOR protein. The effect of KR-9 on HGFs migration and proliferation could be reversed by PI3K inhibitor. These results demonstrated that KR-9 peptide facilitated wound healing of palatal mucosa in rats by promoting HGFs migration and proliferation, which was mediated by PI3K/AKT/mTOR signaling pathway. This data proves that KR-9 might be used as a potential agent for wound healing treatment.

The Effect of γ-Aminobutyric Acid Intake on UVB- Induced Skin Damage in Hairless Mice.

The skin, the largest organ in the body, undergoes age-related changes influenced by both intrinsic and extrinsic factors. The primary external factor is photoaging which causes hyperpigmentation, uneven skin surface, deep wrinkles, and markedly enlarged capillaries. In the human dermis, it decreases fibroblast function, resulting in a lack of collagen structure and also decreases keratinocyte function, which compromises the strength of the protective barrier. In this study, we found that treatment with γ-aminobutyric acid (GABA) had no toxicity to skin fibroblasts and GABA enhanced their migration ability, which can accelerate skin wound healing. UVB radiation was found to significantly induce the production of matrix metalloproteinase 1 (MMP-1), but treatment with GABA resulted in the inhibition of MMP-1 production. We also investigated the enhancement of filaggrin and aquaporin 3 in keratinocytes after treatment with GABA, showing that GABA can effectively improve skin moisturization. In vivo experiments showed that oral administration of GABA significantly improved skin wrinkles and epidermal thickness. After the intake of GABA, there was a significant decrease observed in the increase of skin thickness measured by calipers and erythema. Additionally, the decrease in skin moisture and elasticity in hairless mice exposed to UVB radiation was also significantly restored. Overall, this study demonstrates the potential of GABA as functional food material for improving skin aging and moisturizing.

Multi‐Functional Supramolecular‐Polymeric Hybrid Hydrogel for Promoting Cutaneous Wound Repair†

Comprehensive SummarySupramolecular‐polymeric hybrid hydrogels combining advantages of the assembled supramolecular networks and polymeric networks have attracted considerable attention recently. However, they are rarely used as multi‐functional wound dressing materials. In this work, we report a supramolecular‐polymeric hybrid hydrogel consisting of a co‐assembled DBS‐COOH/Naproxen network (DBS/NAP) and a polymeric gelatin (G)/quaternary ammonium group (Q) and phenylboronic acid groups (PBA)‐grafted chitosan (QCS‐PBA) network (G/QCS) for accelerating skin wound healing. The polymeric networks could obviously enhance the mechanical properties of the drug‐derived supramolecular networks. Q groups endowed the hydrogel with enhanced antibacterial properties. Borate ester crosslinking between PBA groups and diol groups in DBS‐COOH could effectively scavenge reactive radicals. The hybrid hydrogel exhibited tunable mechanical and adhesive properties due to the temperature‐responsive gelatin networks. NAP could gradually release from hybrid hydrogel networks thus continuously relieving inflammation. Finally, the biocompatible, adhesive, antibacterial and antioxidant hybrid G/QCS‐DBS/NAP gel could promote the in vivo healing stages in a full‐thickness wounds with increased collagen deposition, upregulated CD31 expression and down‐regulated TNF‐α expression. Overall, this multi‐functional supramolecular‐polymeric hybrid hydrogel exhibited great potential for treating skin defects as promising wound dressing materials.

LSD1 interacting with HSP90 promotes skin wound healing by inducing metabolic reprogramming of hair follicle stem cells through the c-MYC/LDHA axis.

It has been demonstrated that hair follicle stem cells (HFSCs) can contribute to wound closure and repair. However, the specific mechanism remains unclear due to the complexity of the wound repair process. Lysine-specific demethylase 1 (LSD1), an important gene for the regulation of stem cell differentiation, has been reported to participate in wound healing regulation. Heat shock protein 90 (HSP90), a chaperone protein, is recently discovered to be a driver gene for wound healing. This study explored the molecular mechanisms by which the binding between LSD1 and HSP90 affects the role of HFSCs during skin wound healing. Following bioinformatics analysis, the key genes acting on HFSCs were identified. The expression of LSD1, HSP90, and c-MYC was found to be upregulated in differentiated HFSCs. Analysis of their binding affinity revealed that LSD1 interacted with HSP90 to enhance the stability of the transcription factor c-MYC. Lactate dehydrogenase A (LDHA) has been documented to be essential for HFSC activation. Therefore, we speculate that LDHA may induce the differentiation of HFSCs through glucose metabolism reprogramming. The results showed that c-MYC activated LDHA activity to promote glycolytic metabolism, proliferation, and differentiation of HFSCs. Finally, in vivo animal experiments further confirmed that LSD1 induced skin wound healing in mice via the HSP90/c-MYC/LDHA axis. From our data, we conclude that LSD1 interacting with HSP90 accelerates skin wound healing by inducing HFSC glycolytic metabolism, proliferation, and differentiation via c-MYC/LDHA axis.

Roles of bovine sialoglycoproteins for anti-skin aging and accelerating skin wound healing.

Fibroblasts are the most predominant cell subpopulation in the dermal layer of human skin, they play an important role in maintaining skin architecture and function. The senescence of fibroblasts is one of major causes of skin aging and chronic wound in the elderly, which is accompanied with a reduction of α2,6-sialylation on the cell surface. In this study, we investigated the effects of the bovine sialoglycoproteins on normal human dermal fibroblasts (NHDF). The results showed that bovine sialoglycoproteins could promote the proliferation and migration of NHDF cells, and accelerate the contraction of fibroblast-populated collagen lattice (FPCL). The average doubling time of NHDF cells treated with bovine sialoglycoproteins (0.5 mg/mL) was 31.1 ± 1.0 h whereas that was 37.9 ± 2.7 h for the control (p ˂ 0.05). Moreover, the expression of basic fibroblast growth factor (FGF-2) was upregulated, while that of transforming growth factor-beta 1 (TGF-β1) and human type I collagen (COL-I) were downregulated in treated NHDF cells. Furthermore, bovine sialoglycoproteins treatment significantly enhanced the α2,6-sialylation on the cell surfaces, which was consistent with the upregulation of α2,6-sialyltransferase I (ST6GAL1) expression. These results indicated that the bovine sialoglycoproteins might be developed as a reagent against skin aging in the cosmetic industry, or as a new candidate for accelerating skin wound healing and inhibiting scar formation.

Valproic acid accelerates skin wound healing in mice via its anti-inflammatory and apoptotic cell clearance-promoting effects.

To investigate the effects of valproic acid (VPA) on skin wound healing in mice. Full-thickness wounds were created in mice, and then VPA was applied. The wound areas were quantified daily. In the wounds, granulation tissue growth, epithelialization, collagen deposition, and the mRNA levels of inflammatory cytokines were measured; furthermore, apoptotic cells were labeled. In vitro, VPA was added to RAW 264.7 cells (macrophages) stimulated with lipopolysaccharide, and apoptotic Jurkat cells were cocultured with the VPA-pretreated macrophages. Then, phagocytosis was analyzed, and the mRNA levels of phagocytosis-associated molecules and inflammatory cytokines were measured in the macrophages. VPA application significantly accelerated wound closure, granulation tissue growth, collagen deposition, and epithelialization. In wounds, the levels of tumor necrosis factor-α, interleukin (IL)-6, and IL-1β were decreased by VPA, whereas those of IL-10 and transforming growth factor-β1 were increased. Additionally, VPA reduced the number of apoptotic cells. In vitro, VPA inhibited the inflammatory activation of macrophages and promoted the phagocytosis of apoptotic cells by macrophages. VPA accelerated skin wound healing, which could be partly attributable to its anti-inflammatory and apoptotic cell clearance-promoting effects, indicating that VPA could be a promising candidate for enhancing skin wound healing.

Preparation of Apoptotic Extracellular Vesicles from Adipose Tissue and Their Efficacy in Promoting High-Quality Skin Wound Healing.

A lot of strategies have been attempted to achieve high-quality skin wound healing, among them, fat transplantation has been used for skin wound repair and scar management and has shown beneficial effects. However, the underlying mechanism is still unclear. Recently, studies found that transplanted cells underwent apoptosis within a short period and apoptotic extracellular vesicles (ApoEVs) might play the therapeutic role. In this study, we directly isolated apoptotic extracellular vesicles from adipose tissue (ApoEVs-AT) and evaluated their characteristics. In vivo, we investigated the therapeutic role of ApoEVs-AT in full-thickness skin wounds. The rate of wound healing, the quality of granulation tissue, and the area of scars were evaluated here. In vitro, we investigated the cellular behaviors of fibroblasts and endothelial cells induced by ApoEVs-AT, including cellular uptake, proliferation, migration, and differentiation. ApoEVs-AT could be successfully isolated from adipose tissue and possessed the basic characteristics of ApoEVs. In vivo, ApoEVs-AT could accelerate skin wound healing, improve the quality of granulation tissue, and reduce the area of scars. In vitro, ApoEVs-AT could be engulfed by fibroblasts and endothelial cells, significantly enhancing their proliferation and migration. Moreover, ApoEVs-AT could promote adipogenic differentiation and inhibit the fibrogenic differentiation of fibroblasts. These findings indicated that ApoEVs could be successfully prepared from adipose tissue and showed the ability to promote high-quality skin wound healing by modulating fibroblasts and endothelial cells.

A novel Fe3O4/CuOx nanozyme: Intrinsic peroxidase-like activity to kill bacteria and sterilize wounds

Herein, we report a Fe3O4/CuOx composite with intrinsic highly peroxidase-like activity. The Fe3O4/CuOx composite maintained high activity in the normal skin pH range (4.0–6.0) and over a wide temperature range (25–60 °C). The prepared Fe3O4/CuOx exhibited good bactericidal properties against Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli) at low H2O2 concentration (100 μM). The composite could also effectively destroy the biological film and prevent the emergence of new bacterial film. In addition, Fe3O4/CuOx was easily separated from the media by external magnets and reused five times while maintaining high antibacterial activity. The predominant free radicals (•OH and 1O2) were identified during the sterilization process using a trapping experiment and electron spin resonance (ESR). In addition, the dressing of Fe3O4/CuOx was designed to accelerate skin wound healing, maintaining good cytocompatibility significantly. This composite Fe3O4/CuOx is promising for a wide range of uses in bacterial management.

Mesenchymal stem cell-derived secretomes-enriched alginate/ extracellular matrix hydrogel patch accelerates skin wound healing

BackgroundThe secretomes of mesenchymal stem cells (MSCs) have great therapeutic potential and thereby their efficient delivery into the target site is of particular interest. Here, we propose a new strategy of hMSCs-derived secretomes delivery for advanced wound healing upon harnessing the working principle of extracellular matrix (ECM)-growth factors interaction in vivo.MethodsWe prepared an alginate hydrogel based wound patch, where it contains both human MSC-derived secretomes and ECM. The ECM was obtained from the decellularization of in vitro cultured human lung fibroblasts. The alginate solution was blended with ECM suspension, crosslinked, air-dried, then rehydrated with the secretomes contained in the concentrated conditioned media (CCM) as a highly saturated form of conditioned media (CM). We tested four different groups, with or without the ECM to investigate not only the role of ECM but the therapeutic effect of secretomes.ResultsThe secretomes reserved many, diverse bioactive factors, such as VEGF, HGF, IGFBPs, IL-6, and IL-8. Alginate/ECM/CCM (AEC) patch could hold significantly larger amount of secretomes and release them longer than the other groups. Our AEC patch was the most effective in stimulating not only cell migration and proliferation but the collagen synthesis of dermal fibroblasts in vitro. Moreover, the AEC patch-treated full-thickness skin wounds disclosed significantly better wound healing indications: cell recruitment, neovascularization, epidermis thickness, keratinocyte migration, and mature collagen deposition, as assessed via histology (H&E, Herovici staining) and immunofluorescence, respectively. In particular, our AEC patch enabled a phenotype shift of myofibroblast into fibroblast over time and led to mature blood vessel formation at 14 day.ConclusionsWe believe that ECM certainly contributed to generate a secretomes-enriched milieu via ECM-secretomes interactions and thereby such secretomes could be delivered more efficiently, exerting significant therapeutic impact either individually or collectively during wound healing process.Graphical abstract

An Ultrasound-Driven Bioadhesive Triboelectric Nanogenerator for Instant Wound Sealing and Electrically Accelerated Healing in Emergencies.

A bioadhesive triboelectric nanogenerator (BA-TENG), as a first-aid rescue for instant and robust wound sealing and ultrasound-driven accelerated wound healing, is designed. This BA-TENG is fabricated with biocompatible materials, and integrates a flexible TENG as the top layer and bioadhesive as the bottom layer, resulting in effective electricity supply and strong sutureless sealing capability on wet tissues. When driven by ultrasound, the BA-TENG can produce a stable voltage of 1.50V and current of 24.20µA underwater. The ex vivo porcine colon organ models show that the BA-TENG seals defects instantly (≈5 s) with high interfacial toughness (≈150 J m-2 ), while the rat bleeding liver incision model confirms that the BA-TENG performs rapid wound closure and hemostasis, reducing the blood loss by about 82%. When applied in living rats, the BA-TENG not only seals skin injuries immediately but also produces a strong electric field (E-field) of about 0.86kV m-1 stimulated by ultrasound to accelerate skin wound healing significantly. The in vitro studies confirm that these effects are attributed to the E-field-accelerated cell migration and proliferation. In addition, these TENG adhesives can be applied to not only wound treatment, nerve stimulation and regeneration, and charging batteries in implanted devices.

Green polymer hydrogels from a natural monomer with inherent antioxidative capability for efficient wound healing and spinal cord injury treatment.

Development of polymeric hydrogels with multiple functions (adhesiveness, self-healability, anti-oxidation efficiency, etc.) through one-step green polymerization of naturally occurring small molecules in water is critical for various biomedical applications and clinical transformation. In this work, benefiting from the dynamic disulfide bond in α-lipoic acid (LA), we directly obtain an advanced hydrogel (poly(lipoic acid-co-sodium lipoate) (PLAS)) through heat and concentration-induced ring-opening polymerization of LA with the addition of NaHCO3 in an aqueous solution. The presence of COOH, COO- and disulfide bonds endows the resulting hydrogels with comprehensive mechanical properties, facile injectability, fast self-healability and adequate adhesiveness. Moreover, the PLAS hydrogels show promising antioxidative efficiency, inherited from naturally occurring LA, and can efficiently eliminate intracellular reactive oxygen species (ROS). We also verify the advantage of PLAS hydrogels in a rat spinal injury model. Through the regulation of ROS and in situ inflammation, our system can promote the recovery of spinal cord injury. Owing to the natural origin and inherent anti-oxidative capability of LA, and a green preparation method, our hydrogel should be beneficial for clinical transformation and may be a good candidate for various biomedical applications.

Interpretation of 2020 edition of Japanese "Guidelines for the management of connective tissue disease/vasculitis-associated skin ulcers"

Patients with connective tissue diseases and vasculitis often develop refractory skin ulcers in various parts of the body due to abnormal autoimmune reactions, and the skin ulcers caused by different types of diseases have strong heterogeneity. In 2020, The Journal of Dermatology published the Japanese "Guidelines for the management of connective tissue disease/vasculitis-associated skin ulcers", which is an updated version of its 2016 edition, to guide clinical management of related diseases in a more scientific and standard way. By interpreting the guidelines, this paper aims to help domestic clinicians clarify the diagnosis and treatment objectives of connective tissue disease and vasculitis-associated skin ulcers, accelerate skin wound healing, and improve healing quality.