Preparation of a Coal-Based MoS2/SiO2/GO Composite Catalyst and Its Performance in the Photocatalytic Degradation of Wastewater and Hydrogen Production.

Photocatalytic degradation of wastewater and the simultaneous production of hydrogen (H2) is a green and efficient method to solve energy and environmental problems. In this paper, coal-based SiO2/GO with a stable structure was prepared by a modified Hummers oxidation method, and then, a lotus-shaped composite photocatalyst, MoS2/SiO2/GO, was prepared by in situ loading of flower cluster MoS2 from sodium molybdate reduction onto SiO2/GO. Its photocatalytic degradation of wastewater and H2 production properties were investigated while characterizing the material structure. The results show that SiO2/GO as a carrier not only ensures adequate dispersion of MoS2 but also enhances the visible-light response of the composite catalyst. In addition, it can also hinder the recombination of photogenerated electrons and holes in MoS2 and act as an electron transport channel in composite catalysts. MoS2/SiO2/GO exhibits much higher photocatalytic degradation of wastewater and H2 production capacity than MoS2: after 180 min of reaction, the CODcr removal of wastewater increased from 45.6% for MoS2 to 84.2% for MoS2/SiO2/GO and the H2 yield reached 233.4 µmol. The goal of degrading wastewater while producing H2 more economically has been tentatively achieved, although not to the extent required for industrialization.

Low-level Nd:YAG laser inhibiting inflammation and oxidative stress in human gingival fibroblasts via AMPK/SIRT3 axis.

OBJECTIVE: Photobiomodulation is extensively employed in the management of chronic inflammatory diseases such as periodontitis because of its anti-inflammatory and antioxidant effects. This study used low-level Nd:YAG laser to investigate the mechanism of photobiomodulation as well as the role of adenosine monophosphate-activated protein kinase (AMPK) and Sirtuins (SIRT) 3 in it, providing new clues for the treatment of periodontitis. METHODS: Human gingival fibroblasts (HGFs) were extracted from gingiva and stimulated with LPS. The suitable parameters of Nd:YAG laser were chosen for subsequent experiments by detecting cell viability. We assessed the level of inflammation and oxidative stress as well as AMPK and SIRT3. The mechanism for AMPK targeting SIRT3 modulating the anti-inflammatory and antioxidant effects of photobiomodulation was explored by the AMPK inhibitor (Compound C) test, cell transfection, western blot, and immunofluorescence. RESULTS: HGFs were isolated and identified, followed by the identification of optimal Nd:YAG laser parameters (60 mJ, 15 Hz, 10s) for subsequent experimentation. With this laser, inflammatory factors (IL-6, TNF-α, COX2, and iNOS) decreased as well as the phosphorylation and nuclear translocation of NFκB-P65. SOD2 was up-regulated but reactive oxygen species (ROS) was down-regulated. The laser treatment exhibited enhancements in AMPK phosphorylation and SIRT3 expression. The above effects could all be reversed by Compound C. Silencing AMPK or SIRT3 by siRNA, the down-regulation of COX2, iNOS, and ROS by laser was inhibited. SIRT3 was down-regulated when the AMPK was silenced. CONCLUSION: Low-level Nd:YAG laser activated AMPK-SIRT3 signaling pathway, facilitating the anti-inflammatory and antioxidative activity.

Osteoblasts-Derived Exosomal lncRNA-MALAT1 Promotes Osteoclastogenesis by Targeting the miR-124/NFATc1 Signaling Axis in Bone Marrow-Derived Macrophages.

Objective: Emerging studies have explained the crucial role of non-coding RNA (lncRNA) in various pathological progressions. The study was designed to examine the role of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and miRNA-124 in the differentiation of osteoclasts, to provide new clues or evidences for the pathogenesis of periodontitis. Methods: We constructed an osteoblast-osteoclast Transwell co-culture system and osteoblast-derived exosomes (OB-exo) intervention model. We assessed the osteoclastogenesis as well as the level of lncRNA-MALAT1 and miRNA-124. The mechanism for lncRNA MALAT1 targeting miR-124 modulating the differentiation of osteoclasts was investigated by cell transfection, quantitative real-time reverse transcription PCR (RT-qPCR), Western blot, and Dual-Luciferase reporter assays. Results: Osteoblast-derived exosomes were isolated and identified. Co-culture and OB-exo intervention can promote osteoclastogenesis, also significantly up-regulate the expression of MALAT1, while the level of miR-124 is the opposite. Transfection of cells with small interfering RNA (si-MALAT1) and miR-124 mimic decreased the formation of TRAP+ osteoclasts and inhibited the expression of NFATc1. However, the effect was reversed when transfected with miR-124 inhibitor and si-MALAT1. The Dual-Luciferase reporter assay confirmed the binding sites between MALAT1 and miR-124, and miR-124 and NFATc1. Conclusion: LncRNA MALAT1 functioned as an endogenous sponge by competing for miR-124 binding to regulate NFATc1 expression, accelerating the progression of osteoclastogenesis.

Osteoclast-Derived Exosomal miR-5134-5p Interferes with Alveolar Bone Homeostasis by Targeting the JAK2/STAT3 Axis.

Background: In chronic periodontitis, exosomes transport various informative substances between osteoclasts and osteoblasts in alveolar bone. Herein, we aimed to investigate the effect of exosomal micro-ribonucleic acid (miRNA/miR)-5134-5p derived from osteoclasts on osteoblastic proliferation and differentiation and the development of periodontitis in vivo and in vitro. Methods: The effects of OC-Exos on the proliferation and differentiation of osteoblasts were identified by Real-time quantitative reverse polymerase chain reaction (qRT-PCR), Western blot(WB), alkaline phosphatase(ALP) staining, etc. Exosomal miRNA expression was analyzed by sequencing. The sites of miRNA action were predicted through TargetScan and tested by double luciferase assay. After transfecting miR-5134-5p mimic/inhibitor into osteoblasts, we measured the proliferation and differentiation of osteoblasts by ALP staining and WB, etc. Furthermore, OC-Exos were injected into the gingival sulcus at the ligation site. Inflammation was observed by Hematoxylin-eosin (H&E) staining, the expression of inflammatory factors were detected by qRT-PCR, the resorption of alveolar bone was observed by Micro CT. Results: Osteoblastic proliferation and differentiation were negatively regulated by OC-Exos in vitro. miRNA sequencing analysis revealed that miR-5134-5p expression was significantly elevated in OC-Exos, which also increased in osteoblasts following OC-Exo intervention. The dual-luciferase assay revealed that miR-5134-5p and Janus kinase 2 (JAK2) had binding sites. miR-5134-5p-mimics could upregulate miR-5134-5p expression in osteoblasts while downregulating Runt-related transcription factor 2(Runx2), phosphorylated-JAK2 (p-JAK2), and phosphorylated-signal transducer and activator of transcription 3 (p-STAT3) expression and inhibited osteogenic differentiation. However, miR-5134-5p-inhibitor had the opposite effect. In vivo, the OC-Exo group demonstrated morphological disruption of periodontal tissue, massive inflammatory cell infiltration, upregulation of inflammatory factors mRNA expression, a significant decrease in BV/TV, and an increase in the cementoenamel junction and alveolar bone crest distance. Conclusion: Osteoclast-derived exosomal miR-5134-5p inhibits osteoblastic proliferation and differentiation via the JAK2/STAT3 pathway. OC-Exos exacerbate periodontal tissue inflammation and accelerate alveolar bone resorption in mice with experimental periodontitis.