Matrix Degradation Research Articles

Photocatalytic Performance of the BaSn-based Nanoscale Materials for the Organic Pollutants Enhanced by Sm (Er) Doping

Background: Sm (Er) doping is an effective strategy for enhancing the photocatalytic activity of the semiconductor photocatalysts for the degradation of organic pollutants. BaSnbased nanorods possess wide band gap energy, which limits the photocatalytic application. It is important to research the feasibility of the improved photocatalytic performance of the BaSnbased nanorods by doping with Sm (Er). Objective: The aim is to synthesize Sm (Er)-doped BaSn-based nanoscale materials through a simple hydrothermal process and research the photocatalytic performance of the Sm (Er)-doped BaSn-based nanoscale materials for the gentian violet degradation. Methods: Sm (Er)-doped BaSn-based nanoscale materials with a polycrystalline structure were synthesized through a simple hydrothermal process. The Sm (Er)-doped composites were analyzed by X-ray diffraction, electron microscopy, solid diffuse reflectance spectrum, X-ray photoelectron spectroscopy, photoluminescence, and electrochemical impedance spectroscopy. Results: Sm (Er) doping induces the morphological evolution of the BaSn-based nanoscale materials from the nanorods to irregular nanoscale particles. Sm (Er) in the doped BaSn-based nanoscale materials exists in the form of the cubic Sm2Sn2O7 and orthorhombic ErF3 phases. The band gap value is decreased with increasing the Sm (Er) dopant contents. Sm (Er)-doped BnSnbased nanoscale materials with the Sm (Er) content of 8wt.% have the lowest band gap and show the strongest light absorption ability. Compared with the un-doped BaSn-based nanoscale materials, the Sm (Er)-doped BnSn-based nanoscale materials exhibit higher photocatalytic activity for the gentian violet degradation. 8wt.% Sm-doped BnSn-based nanoscale materials show the highest photocatalytic activity for the degradation of the gentian violet. 20 mL gentian violet solution (concentration of 10 mg·L-1) can be totally degraded using 20 mg 8wt.% Sm-doped BnSnbased nanoscale materials under UV light illumination for 150 min. Conclusion: The enhanced photocatalytic activity of the Sm (Er)-doped BnSn-based nanoscale materials can be attributed to the decreased band gap, enhanced light absorption ability, and decreased recombination of the photo-generated electron-hole pairs.

AMPK/Autophagy-Mediated Alleviation of Tendinopathy by IL-38: A Novel Strategy for the Treatment of Obesity-Related Tendinopathy

The effect of interleukin-38 (IL-38), a recently identified member of the IL-1 family with potential applications in various inflammation-related conditions, on ER stress has not been explored. Furthermore, its role in obesity-associated tendinopathy has not been investigated. In this study, human primary tenocytes were treated with palmitate (200 or 400μM) and palmitate plus IL-38 (0-50ng/mL) for 24h. Western blotting was used to assess ER stress and tendinopathogenic markers in tenocytes. Monodansylcadaverine (MDC) staining was used to evaluate autophagosomes. Apoptosis was determined by cell viability assays, caspase 3 activity assays and TUNEL assays. Cell migration was evaluated by a cell scratch assay. Small interfering (si) RNA transfection was used for target gene silencing. Treatment of tenocytes with IL-38 attenuated apoptosis, restored the balance between MMPs and TIMP-1, and alleviated ER stress under palmitate conditions. IL-38 treatment enhanced AMPK phosphorylation and promoted the expression of autophagy markers related to LC3 conversion, p62 degradation, and autophagosome formation in cultured tenocytes. The effects of IL-38 on ER stress, apoptosis, and MMP-9, MMP-13, and TIMP-1 expression in palmitate-treated tenocytes were abrogated by AMPK siRNA or 3-methyladenine (3MA). These results suggest that IL-38 alleviates ER stress through the AMPK/autophagy pathway, thereby reducing apoptosis and preventing extracellular matrix (ECM) degradation in tenocytes under hyperlipidemic conditions. This study provides a promising therapeutic avenue for treating obesity-related tendinopathy using an endogenous compound such as IL-38.

Recent Advances in Biomedical Nanotechnology Related to Natural Products.

Natural product processing via nanotechnology has opened the door to innovative and significant applications in medical fields. On one hand, plants-derived bioactive ingredients such as phenols, pentacyclic triterpenes and flavonoids exhibit significant pharmacological activities, on another hand, most of them are hydrophobic in nature, posing challenges to their use. To overcome this issue, nanoencapsulation technology is employed to encapsulate these lipophilic compounds and enhance their bioavailability. In this regard, various nano-sized vehicles, including degradable functional polymer organic compounds, mesoporous silicon or carbon materials, offer superior stability and retention for bioactive ingredients against decomposition and loss during delivery as well as sustained release. On the other hand, some naturally occurring polymers, lipids and even microorganisms, which constitute a significant portion of Earth's biomass, show promising potential for biomedical applications as well. Through nano-processing, these natural products can be developed into nano-delivery systems with desirable characteristics for encapsulation a wide range of bioactive components and therapeutic agents, facilitating in vivo drug transport. Beyond the presentation of the most recent nanoencapsulation and nano-processing advancements with formulations mainly based on natural products, this review emphasizes the importance of their physicochemical properties at the nanoscale and their potential in disease therapy.

Investigating protease-mediated peptides of inflammation and tissue remodeling as biomarkers associated with flares in psoriatic arthritis.

Psoriatic arthritis (PsA) is an inflammatory arthritis associated with psoriasis. PsA disease involves flares, which are associated with increased joint inflammation and tissue remodeling. There is a need for identifying biomarkers related to PsA disease activity and flares to improve the management of PsA patients and decrease flares. The tissue turnover imbalance that occurs during the inflammatory and fibro-proliferative processes during flares leads to an increased degradation and/or reorganization of the extracellular matrix (ECM), where increased proteolysis plays a key role. Hence, protease-mediated fragments of inflammatory and tissue-remodeling components could be used as markers reflecting flares in PsA patients. A broad panel of protease-mediated biomarkers reflecting inflammation and tissue remodeling was measured in serum and synovial fluid (SF) obtained from PsA patients experiencing flares (acutely swollen joint[s], PsA-flare). In serum, biomarker levels assessed in PsA-flare patients were compared to controls and in early-diagnosed PsA patients not experiencing flares (referred to as PsA without flare). Furthermore, the biomarker levels assessed in SF from PsA-flare patients were compared to the levels in SF of osteoarthritis (OA) patients. In serum, levels of the PRO-C3 and C3M, reflecting formation and degradation of the interstitial matrix, were found significantly elevated in PsA-flare compared to controls and PsA without flare. The remodeling marker of the basement membrane, PRO-C4, was significantly elevated in PsA-flare compared to PsA without flare. The inflammation and immune cell activity related markers, CRPM, VICM, and CPa9-HNE were significantly elevated in PsA-flare patients compared to controls and PsA without flare. In addition, VICM (AUC = 0.71), CPa9-HNE (AUC = 0.89), CRPM (AUC = 0.76), and PRO-C3 (AUC = 0.86) showed good discriminatory performance for separating PsA-flare from PsA without flare. In SF, the macrophage activity marker, VICM, was significantly elevated whereas the type II collagen formation marker, PRO-C2, was significantly reduced in the PsA-flare compared to OA. The combination of five serum markers reflecting type III and IV collagen degradation (C3M and C4M, respectively), type III and VI collagen formation (PRO-C3 and PRO-C6, respectively), and neutrophil activity (CPa9-HNE) showed an excellent discriminatory performance (AUC = 0.98) for separating PsA-flare from PsA without flares. The serum biomarker panel of C3M, C4M, PRO-C3, PRO-C6, and CPa9-HNE reflecting synovitis, enthesitis, and neutrophil activity may serve as novel tool for quantitatively monitoring flares in PsA patients.

Ultrasonication-assisted synthesis of transition metal carbide of MXene: an efficient and promising material for photocatalytic organic dyes degradation of rhodamine B and methylene blue in wastewater.

Water pollutants of non-biodegradable toxic aromatic dye including Methylene blue (MB) and Rhodamine (RhB) are extremely carcinogenic thiazines used in various industries such asleather industry, paper industry, and the dyeing industry. The presence of dyes in wastewater causes severe threats to human health that are responsible for various harmful chronic or acute diseases and also shows an adverse impact on the environment as it reduces transparency and is harmful to water microorganisms. To overcome severe issues, many traditional techniques have been used to remove toxic pollutants, but thesemethods are insufficient to remove chemically stable dyes that remain in the treated wastewater. However, the photocatalytic degradation process is an efficient approach to degrade the dye up to the maximum extent with improved efficiency. Therefore, in this work, a new class of two-dimensional (2D) transition metal carbide of Titanium Carbide (Ti3C2Tx) MXene material was used for the organic dyes degradation such as MB and RhB using a photocatalytic process. A layered structure of hexagonal lattice symmetry of Ti3C2Tx MXene was successfully synthesized from the Titanium Aluminum Carbide ofTi3AlC2 bulk phase using an exfoliation process. Further, the XRD spectrum confirms the transformation of bulk MAX phase having (002) plane at 9.2° to Ti3C2Tx MXene of (002) plane at 8.88° confirms the successful removal of Al layer from MAX phase. A smooth, transparent, thin sheet-like morphology of Ti3C2Txnanosheet sizewere found to be in the range of 70 to 150nm evaluated fromTEM images. Also,no holes or damages in the thin sheets were foundafter the treatment with strong hydrofluoric acid confirms the formationTi3C2Tx layered sheets. The synthesized Ti3C2Tx MXene possesses excellent photocatalytic activity for the degradation of dyes MB, RhB, and mixtures of MB and RhB dyes. MB dye degraded with a degradation percentage efficiency of 99.32% in 30min, while RhB dye was degraded upto98.9% in 30min. Also, experiments were conducted for degradation ofmixture of MB and RhB dyes by UV light, and the degradationpercentage efficiency were found to be 98.9% and 99.75% for mixture of MB and RhB dyein 45min, respectively. Moreover, reaction rate constant (k) was determined for each dye of MB, RhB, and mixtures of MB and RhB and was found to be 0.0215min-1 and 0.0058min-1, and for mixtures, it was 0.0020min-1 and 0.009min-1, respectively.

The Glabridin from Huangqin Decoction Prevents the Development of Ulcerative Colitis into Colitis-Associated Colorectal Cancer by Modulating MMP1/MMP3 Activity

Background and AimHuangqin decoction (HQD) is a Chinese medicine used to treat colitis and colorectal cancer (CRC). However, the specific compounds and mechanisms of HQD remain unclear despite its good curative clinical results. Through bioinformatics, network pharmacology, and experiments, this study aims to explore the progressive mechanisms of colitis-associated colorectal cancer (CAC) from ulcerative colitis (UC) while examining the protective effects of HQD and its compounds against this. MethodsBioinformatics was utilized to identify the hub genes between UC and CRC, and their clinical predictive significance, function, and expression were validated. Employing network pharmacology in combination with hub genes, key targets of HQD for preventing the development of UC into CAC were identified. Molecular docking and molecular dynamics (MD) were utilized to procure compounds that effectively bind to these targets and their transcription factors (TFs). Finally, the expression and mechanism of key targets were demonstrated in mice with UC or CAC. Results(1) Joint analysis of UC and CRC gene sets resulted in 14 hub genes, mainly related to extracellular matrix receptor binding, biological processes in the extracellular matrix, focal adhesion and neutrophil migration; (2) Network pharmacology results show HQD has 133 core targets for treating UC and CRC, acting on extracellular matrix, inflammatory bowel disease, chemical carcinogen receptor activation and other pathways; (3) The intersection of hub genes and core targets yielded two key targets, MMP1 and MMP3; (4) STAT3 is a shared TF of MMP1 and MMP3. (5) Molecular docking and MD verified that the dockings between Glabridin and STAT3/MMP1/MMP3 are stable and reliable; (6) In murine vivo experiments verified that Glabridin reduces inflammation, extracellular matrix degradation, and the occurrence of epithelial-mesenchymal transition to prevent UC transforming into CAC by inhibiting the phosphorylation of STAT3 and regulating the activity of MMP1/3.

Dynamic monitoring soft tissue healing via visualized Gd-crosslinked double network MRI microspheres

By integrating magnetic resonance-visible components with scaffold materials, hydrogel microspheres (HMs) become visible under magnetic resonance imaging(MRI), allowing for non-invasive, continuous, and dynamic monitoring of the distribution, degradation, and relationship of the HMs with local tissues. However, when these visualization components are physically blended into the HMs, it reduces their relaxation rate and specificity under MRI, weakening the efficacy of real-time dynamic monitoring. To achieve MRI-guided in vivo monitoring of HMs with tissue repair functionality, we utilized airflow control and photo-crosslinking methods to prepare alginate-gelatin-based dual-network hydrogel microspheres (G-AlgMA HMs) using gadolinium ions (Gd (III)), a paramagnetic MRI contrast agent, as the crosslinker. When the network of G-AlgMA HMs degrades, the cleavage of covalent bonds causes the release of Gd (III), continuously altering the arrangement and movement characteristics of surrounding water molecules. This change in local transverse and longitudinal relaxation times results in variations in MRI signal values, thus enabling MRI-guided in vivo monitoring of the HMs. Additionally, in vivo data show that the degradation and release of polypeptide (K2 (SL)6 K2 (KK)) from G-AlgMA HMs promote local vascular regeneration and soft tissue repair. Overall, G-AlgMA HMs enable non-invasive, dynamic in vivo monitoring of biomaterial degradation and tissue regeneration through MRI, which is significant for understanding material degradation mechanisms, evaluating biocompatibility, and optimizing material design.

Hydrolytic and soil degradation of cellulosic material (paper): optimization of parameters using ANN and RSM

Hydrolytic and soil degradation of cellulosic material (paper): optimization of parameters using ANN and RSM

VCP/p97 UFMylation stabilizes BECN1 and facilitates the initiation of autophagy

ABSTRACT Macroautophagy/autophagy is essential for the degradation and recycling of cytoplasmic materials. The initiation of this process is determined by phosphatidylinositol-3-kinase (PtdIns3K) complex, which is regulated by factor BECN1 (beclin 1). UFMylation is a novel ubiquitin-like modification that has been demonstrated to modulate several cellular activities. However, the role of UFMylation in regulating autophagy has not been fully elucidated. Here, we found that VCP/p97 is UFMylated on K109 by the E3 UFL1 (UFM1 specific ligase 1) and this modification promotes BECN1 stabilization and assembly of the PtdIns3K complex, suggesting a role for VCP/p97 UFMylation in autophagy initiation. Mechanistically, VCP/p97 UFMylation stabilizes BECN1 through ATXN3 (ataxin 3)-mediated deubiquitination. As a key component of the PtdIns3K complex, stabilized BECN1 facilitates assembly of this complex. Re-expression of VCP/p97, but not the UFMylation-defective mutant, rescued the VCP/p97 depletion-induced increase in MAP1LC3B/LC3B protein expression. We also showed that several pathogenic VCP/p97 mutations identified in a variety of neurological disorders and cancers were associated with reduced UFMylation, thus implicating VCP/p97 UFMylation as a potential therapeutic target for these diseases. Abbreviation: ATG14:autophagy related 14; Baf A1:bafilomycin A1;CMT2Y: Charcot-Marie-Toothdisease, axonal, 2Y; CYB5R3: cytochromeb5 reductase 3; DDRGK1: DDRGK domain containing 1; DMEM:Dulbecco’smodified Eagle’s medium;ER:endoplasmic reticulum; FBS:fetalbovine serum;FTDALS6:frontotemporaldementia and/or amyotrophic lateral sclerosis 6; IBMPFD1:inclusion bodymyopathy with early-onset Paget disease with or withoutfrontotemporal dementia 1; LC-MS/MS:liquid chromatography tandem mass spectrometry; MAP1LC3B/LC3B:microtubule associated protein 1 light chain 3 beta; MS: massspectrometry; NPLOC4: NPL4 homolog, ubiquitin recognition factor;PIK3C3: phosphatidylinositol 3-kinase catalytic subunit type 3;PIK3R4: phosphoinositide-3-kinase regulatory subunit 4; PtdIns3K:phosphatidylinositol 3-kinase; RPL26: ribosomal protein L26; RPN1:ribophorin I; SQSTM1/p62: sequestosome 1; UBA5: ubiquitin likemodifier activating enzyme 5; UFC1: ubiquitin-fold modifierconjugating enzyme 1; UFD1: ubiquitin recognition factor in ERassociated degradation 1; UFL1: UFM1 specific ligase 1; UFM1:ubiquitin fold modifier 1; UFSP2: UFM1 specific peptidase 2; UVRAG:UV radiation resistance associated; VCP/p97: valosin containingprotein; WT: wild-type

Chiral-structured heterointerfaces enable durable perovskite solar cells.

Mechanical failure and chemical degradation of device heterointerfaces can strongly influence the long-term stability of perovskite solar cells (PSCs) under thermal cycling and damp heat conditions. We report chirality-mediated interfaces based on R-/S-methylbenzyl-ammonium between the perovskite absorber and electron-transport layer to create an elastic yet strong heterointerface with increased mechanical reliability. This interface harnesses enantiomer-controlled entropy to enhance tolerance to thermal cycling-induced fatigue and material degradation, and a heterochiral arrangement of organic cations leads to closer packing of benzene rings, which enhances chemical stability and charge transfer. The encapsulated PSCs showed retentions of 92% of power-conversion efficiency under a thermal cycling test (-40°C to 85°C; 200 cycles over 1200 hours) and 92% under a damp heat test (85% relative humidity; 85°C; 600 hours).

Endothelin and the tumor microenvironment: a finger in every pie.

The tumor microenvironment (TME) plays a central role in the development of cancer. Within this complex milieu, the endothelin (ET) system plays a key role by triggering epithelial-to-mesenchymal transition, causing degradation of the extracellular matrix and modulating hypoxia response, cell proliferation, composition, and activation. These multiple effects of the ET system on cancer progression have prompted numerous preclinical studies targeting the ET system with promising results, leading to considerable optimism for subsequent clinical trials. However, these clinical trials have not lived up to the high expectations; in fact, the clinical trials have failed to demonstrate any substantiated benefit of targeting the ET system in cancer patients. This review discusses the major and recent advances of the ET system with respect to TME and comments on past and ongoing clinical trials of the ET system.

Remodeling and Regenerative Properties of Fully Absorbable Meshes for Abdominal Wall Defect Repair: A Systematic Review and Meta-Analysis of Animal Studies.

Fully absorbable meshes can repair abdominal wall defects and effectively reduce the incidence of complications, but different types of fully absorbable meshes have different remodeling and regeneration effects. In order to investigate and compare the effects of different fully absorbable meshes on remodeling and regeneration in animals and reduce the biological risk of clinical translation, SYRCLE was adopted to evaluate the methodological quality of the included studies, and GRADE and ConQual were used to evaluate the quality of evidence. According to the inclusion and exclusion criteria, a total of 22 studies related to fully absorbable meshes were included in this systematic review. These results showed that fiber-based synthetic materials and fiber-based natural materials exhibited better restorative and regenerative effects indicated by infiltration and neovascularization, when compared with a porcine acellular dermal matrix. In addition, the human acellular dermal matrix was found to have a similar regenerative effect on the host extracellular matrix and scaffold degradation compared to the porcine acellular dermal matrix, porcine intestinal submucosa, and fiber-based natural materials, but it offered higher tensile strength than the other three. The quality of the evidence in this field was found to be poor. The reasons for downgrading were analyzed, and recommendations for future research included more rigor in study design, more transparency in result reporting, more standardization of animal models and follow-up time for better evaluation of the remodeling and regenerative performance of abdominal wall hernia repair meshes, and less biological risk in clinical translation.

Nrf2 activation by pyrroloquinoline quinone inhibits natural aging-related intervertebral disk degeneration in mice.

Age-related intervertebral disk degeneration (IVDD) involves increased oxidative damage, cellular senescence, and matrix degradation. Pyrroloquinoline quinone (PQQ) is a water-soluble vitamin-like compound with strong anti-oxidant capacity. The goal of this study was to determine whether PQQ can prevent aging-related IVDD, and the underlying mechanism. Here, we found that dietary PQQ supplementation for 12 months alleviated IVDD phenotypes in aged mice, including increased disk height index and reduced histological scores and cell loss, without toxicity. Mechanistically, PQQ inhibited oxidative stress, cellular senescence, and senescence-associated secretory phenotype (SASP) in the nucleus pulposus and annulus fibrosus of aged mice. Similarly, PQQ protected against interleukin-1β-induced matrix degradation, reactive oxygen species accumulation, and senescence in human nucleus pulposus cells (NPCs) invitro. Molecular docking predicted and biochemical assays validated that PQQ interacts with specific residues to dissociate the Keap1-Nrf2 complex, thereby increasing nuclear Nrf2 translocation and activation of Nrf2-ARE signaling. RNA sequencing and luciferase assays revealed Nrf2 can transcriptionally upregulate Wnt5a by binding to its promoter, while Wnt5a knockdown prevented PQQ inhibition of matrix metalloproteinase-13 in NPCs. Notably, PQQ supplementation failed to alleviate aging-associated IVDD phenotypes and oxidative stress in aged Nrf2 knockout mice, indicating Nrf2 is indispensable for PQQ bioactivities. Collectively, this study demonstrates Nrf2 activation by PQQ inhibits aging-induced IVDD by attenuating cellular senescence and matrix degradation. This study clarifies Keap1-Nrf2-Wnt5a axis as the novel signaling underlying the protective effects of PQQ against aging-related IVDD, and provides evidence for PQQ as a potential agent for clinical prevention and treatment of natural aging-induced IVDD.

Polymer-Based Immobilized FePMo12O40@PVP Composite Materials for Photocatalytic RhB Degradation

Polymer-Based Immobilized FePMo12O40@PVP Composite Materials for Photocatalytic RhB Degradation

Engineered K-doped ZnO/borneol based hydrogel composite material for led-based photocatalytic degradation of methylene blue and evaluation of antimicrobial activity

Engineered K-doped ZnO/borneol based hydrogel composite material for led-based photocatalytic degradation of methylene blue and evaluation of antimicrobial activity

Spinosin ameliorates osteoarthritis through enhancing the Nrf2/HO-1 signaling pathway.

Osteoarthritis (OA) is a common degenerative joint disease in the elderly, while oxidative stress-induced chondrocyte degeneration plays a key role in the pathologic progression of OA. One possible reason is that theexpression of nuclear factor erythroid 2-related factor 2 (Nrf2), which acts as the intracellular defense factor against oxidative stress, is significantly inhibited in chondrocytes. Spinosin (SPI) is a potent Nrf2 agonist, butits effect on OA is still unknown. In this study, we found that SPI can alleviate tert-Butyl hydroperoxide (TBHP)-induced extracellular matrix degradation of chondrocytes. Additionally, SPI can effectively activateNrf2, heme oxygenase-1 (HO-1), and NADPH quinone oxidoreductase 1 (NQO1) in chondrocytes under theTBHP environment. When Nrf2 was silenced by siRNA, the cartilage protective effect of SPI was also weakened.Finally, SPI showed good alleviative effects on OA in mice. Thus, SPI can ameliorate oxidative stress-induced chondrocyte dysfunction and exhibit a chondroprotective effect through activating the Nrf2/HO-1pathway, which may provide a novel and promising option for the treatment of OA.

Inhibition of miR-199b-5p reduces pathological alterations in osteoarthritis by potentially targeting Fzd6 and Gcnt2

Osteoarthritis (OA) is a degenerative disease with a high prevalence in the elderly population, but our understanding of its mechanisms remains incomplete. Analysis of serum exosomal small RNA sequencing data from clinical patients and gene expression data from OA patient serum and cartilage obtained from the GEO database revealed a common dysregulated miRNA, miR-199b-5p. In vitro cell experiments demonstrated that miR-199b-5p inhibits chondrocyte vitality and promotes extracellular matrix degradation. Conversely, inhibition of miR-199b-5p under inflammatory conditions exhibited protective effects against damage. Local viral injection of miR-199b-5p into mice induced a decrease in pain threshold and OA-like changes. In an OA model, inhibition of miR-199b-5p alleviated the pathological progression of OA. Furthermore, bioinformatics analysis and experimental validation identified Gcnt2 and Fzd6 as potential target genes of MiR-199b-5p. Thus, these results indicated that MiR-199b-5p/Gcnt2 and Fzd6 axis might be a novel therapeutic target for the treatment of OA.

Inhibition of miR-199b-5p reduces pathological alterations in osteoarthritis by potentially targeting Fzd6 and Gcnt2.

Osteoarthritis (OA) is a degenerative disease with a high prevalence in the elderly population, but our understanding of its mechanisms remains incomplete. Analysis of serum exosomal small RNA sequencing data from clinical patients and gene expression data from OA patient serum and cartilage obtained from the GEO database revealed a common dysregulated miRNA, miR-199b-5p. In vitro cell experiments demonstrated that miR-199b-5p inhibits chondrocyte vitality and promotes extracellular matrix degradation. Conversely, inhibition of miR-199b-5p under inflammatory conditions exhibited protective effects against damage. Local viral injection of miR-199b-5p into mice induced a decrease in pain threshold and OA-like changes. In an OA model, inhibition of miR-199b-5p alleviated the pathological progression of OA. Furthermore, bioinformatics analysis and experimental validation identified Gcnt2 and Fzd6 as potential target genes of MiR-199b-5p. Thus, these results indicated that MiR-199b-5p/Gcnt2 and Fzd6 axis might be a novel therapeutic target for the treatment of OA.

Impact of vitamin D on ultraviolet-induced photoaging and skin diseases

Excessive exposure to ultraviolet (UV) radiation causes premature aging of the skin, known as photoaging. UV radiation induces DNA damage, oxidative stress, inflammatory reactions, and degradation of extracellular matrix (ECM) proteins, contributing to the aged skin phenotype. The skin synthesizes vitamin D upon UVB exposure, which plays a pivotal role in the proper function of multiple body systems. Vitamin D protects skin from photo-damage by repairing cyclobutane pyrimidine dimers, reversing oxidative stress, and reducing chronic inflammation. Moreover, various epidemiological studies have identified vitamin D deficiency as a marker for common dermatological disorders. Improvement of clinical outcomes with vitamin D supplementation further suggests its protective role against skin pathologies. This review comprehensively covers the involvement of vitamin D in combating UV-induced photoaging and various skin disorders, highlighting the significance of maintaining vitamin D adequacy for healthy skin.

LaCoO3@Fe3O4 as peroxymonosulfate activator derived from spent lithium battery cathode materials for degradation of sulfamethoxazole in water

To reduce the various hazards of SMX to aquatic ecosystems, in this study, magnetically separable LaCoO3@Fe3O4 catalysts for the degradation of sulfamethoxazole (SMX) in water by activated peroxymonosulfate (PMS) were successfully prepared by using cobalt oxalate recovered from spent batteries using sol–gel, hydrothermal, and high-temperature calcination methods. The main factors influencing the reaction and the effect of coexisting ions on the degradation efficiency of SMX were investigated. The results showed that under optimal conditions ([SMX] = 30 mg, [LaCoO3@Fe3O4] = 10 mg/L, [PMS] = 30 mg/L, pH (initial) = 7.02), the LaCoO3@Fe3O4/PMS system degraded SMX up to 93 % in 15 min. The degradation of SMX in the LaCoO3@Fe3O4/PMS system was shown to be achieved by a combination of radical (SO4•-/•OH/•O2–) and non-radical (1O2) pathways by quenching experiments and electron paramagnetic resonance spectroscopy (EPR) analysis. Then, three possible degradation pathways were proposed using LC-MS, and Ecological Constitutive Relationship (ECOSAR) analysis showed that the toxicity of the intermediate products was all lower than that of SMX, indicating that the system is feasible for SMX degradation. This study provides a new idea for activating PMS for the degradation of antibiotics in water by preparing catalysts using precious metals from recycled batteries.