ABSTRACT
Skeletal fluorosis is a chronic metabolic bone disease caused by long-term excessive fluoride intake. Abnormal differentiation of osteoblasts plays an important role in disease progression. Research on the mechanism of fluoride-mediated bone differentiation is necessary for the prevention and treatment of skeletal fluorosis. In the present study, a rat model of fluorosis was established by exposing it to drinking water containing 50 mg/L F-. We found that fluoride promoted Runt-related transcription factor 2 (RUNX2) as well as superoxide dismutase 2 (SOD2) and sirtuin 3 (SIRT3) expression in osteoblasts of rat bone tissue. In vitro, we also found that 4 mg/L sodium fluoride promoted osteogenesis-related indicators as well as SOD2 and SIRT3 expression in MG-63 and Saos-2 cells. In addition, we unexpectedly discovered that fluoride suppressed the levels of reactive oxygen species (ROS) and mitochondrial reactive oxygen species (mtROS) in osteoblasts. When SOD2 or SIRT3 was inhibited in MG-63 cells, fluoride-decreased ROS and mtROS were alleviated, which in turn inhibited fluoride-promoted osteogenic differentiation. In conclusion, our results suggest that SIRT3/SOD2 mediates fluoride-promoted osteoblastic differentiation by down-regulating reactive oxygen species.
ABSTRACT
Two-dimensional (2D) metal halide perovskites, such as BA2SnI4 (BAâCH3(CH2)3NH3), exhibit an enhanced charge carrier lifetime in experiments under strain. Experiments suggest that significant compression of the BA molecule, rather than of the inorganic lattice, contributes to this enhancement. To elucidate the underlying physical mechanism, we apply a moderate compressive strain to the entire system and subsequently introduce significant compression to the BA molecules. We then perform ab initio nonadiabatic molecular dynamics simulations of nonradiative electron-hole recombination. We observe that the overall lattice compression reduces atomic motions and decreases nonadiabatic coupling, thereby delaying electron-hole recombination. Additionally, compression of the BA molecules enhances hydrogen bonding between the BA molecules and iodine atoms, which lengthens the Sn-I bonds, distorts the [SnI6]4- octahedra, and suppresses atomic motions further, thus reducing nonadiabatic coupling. Also, the elongated Sn-I bonds and weakened antibonding interactions increase the band gap. Altogether, the compression delays the nonradiative electron-hole recombination by more than a factor of 3. Our simulations provide new and valuable physical insights into how compressive strain, accommodated primarily by the organic ligands, positively influences the optoelectronic properties of 2D layered halide perovskites, offering a promising pathway for further performance improvements.
ABSTRACT
Catheter-associated urinary tract infection (CAUTI) is a common clinical problem, especially during long-term catheterization, causing additional pain to patients. The development of novel antimicrobial coatings is needed to prolong the service life of catheters and reduce the incidence of CAUTIs. Herein, we designed an antimicrobial catheter coated with a piezoelectric zinc oxide nanoparticles (ZnO NPs)-incorporated polyvinylidene difluoride-hexafluoropropylene (ZnO-PVDF-HFP) membrane. ZnO-PVDF-HFP could be stably coated onto silicone catheters simply by a one-step solution film-forming method, very convenient for industrial production. In vitro, it was demonstrated that ZnO-PVDF-HFP coating could significantly inhibit bacterial growth and the formation of bacterial biofilm under ultrasound-mediated mechanical stimulation even after 4 weeks. Importantly, the on and off of antimicrobial activity as well as the strenth of antibacterial property could be controlled in an adaptive manner via ultrasound. In a rabbit model, the ZnO-PVDF-HFP-coated catheter significantly reduced the incidence CAUTIs compared with clinically-commonly used catheters under assistance of ultrasonication, and no side effect was detected. Collectively, the study provided a novel antibacterial catheter to prevent the occurrence of CAUTIs, whose antibacterial activity could be controlled in on-demand manner, adaptive to infection situation and promising in clinical application.
ABSTRACT
In this study, blueberry anthocyanins extract (BAE) was used to investigate its protective effect on arsenic-induced rat hippocampal neurons damage. Arsenic exposure resulted in elevated levels of oxidative stress, decreased antioxidant capacity and increased apoptosis in rat hippocampal brain tissue and mitochondria. Immunohistochemical results showed that arsenic exposure also significantly decreased the expression of mitochondrial biosynthesis-related factors PGC-1α and TFAM. Treatment with BAE alleviated the decrease in antioxidant capacity, mitochondrial biogenesis related protein PGC-1α/NRF2/TFAM expression, and ATP production of arsenic induced hippocampal neurons in rats, and improved cognitive function in arsenic damaged rats. This study provides new insights into the detoxification effect of anthocyanins on the nervous system toxicity caused by metal exposure in the environment, indicating that anthocyanins may be a natural antioxidant against the nervous system toxicity caused by environmental metal exposure.
Subject(s)
Anthocyanins , Arsenic , Blueberry Plants , Hippocampus , Memory Disorders , Mitochondria , NF-E2-Related Factor 2 , Neurons , Oxidative Stress , Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha , Animals , Blueberry Plants/chemistry , Oxidative Stress/drug effects , Hippocampus/metabolism , Hippocampus/drug effects , Arsenic/toxicity , Neurons/drug effects , Neurons/metabolism , Mitochondria/metabolism , Mitochondria/drug effects , Anthocyanins/pharmacology , Rats , Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism , Memory Disorders/chemically induced , Memory Disorders/metabolism , Memory Disorders/drug therapy , NF-E2-Related Factor 2/metabolism , Antioxidants/pharmacology , Male , DNA-Binding Proteins/metabolism , Apoptosis/drug effects , Transcription Factors/metabolism , Rats, Sprague-Dawley , Plant Extracts/pharmacologyABSTRACT
Infiltration of excessive antibiotics into aquatic ecosystems plays a significant role in antibiotic resistance, a major global health challenge. It is therefore critical to develop effective technologies for their removal. Herein, defect-rich Bi2WO6 nanoparticles are solvothermally prepared via epitaxial growth on pristine Bi2WO6 seed nanocrystals, and the efficiency of the photocatalytic degradation of ciprofloxacin, a common antibiotic, is found to increase markedly from 62.51% to 98.27% under visible photoirradiation for 60 min. This is due to the formation of a large number of structural defects, where the synergistic interactions between grain boundaries and adjacent dislocations and oxygen vacancies lead to an improved separation and migration efficiency of photogenerated carriers and facilitate the adsorption and degradation of ciprofloxacin, as confirmed in experimental and theoretical studies. Results from this work demonstrate the unique potential of defect engineering for enhanced photocatalytic performance, a critical step in removing antibiotic contaminants in aquatic ecosystems.
Subject(s)
Anti-Bacterial Agents , Bismuth , Anti-Bacterial Agents/chemistry , Bismuth/chemistry , Catalysis , Ciprofloxacin/chemistry , Nanoparticles/chemistry , Tungsten/chemistry , OxidesABSTRACT
Pulsed electromagnetic field (PEMF) stimulation is a prospective non-invasive and safe physical therapy strategy for accelerating bone repair. PEMFs can activate signalling pathways, modulate ion channels, and regulate the expression of bone-related genes to enhance osteoblast activity and promote the regeneration of neural and vascular tissues, thereby accelerating bone formation during bone repair. Although their mechanisms of action remain unclear, recent studies provide ample evidence of the effects of PEMF on bone repair. In this review, we present the progress of research exploring the effects of PEMF on bone repair and systematically elucidate the mechanisms involved in PEMF-induced bone repair. Additionally, the potential clinical significance of PEMF therapy in fracture healing is underscored. Thus, this review seeks to provide a sufficient theoretical basis for the application of PEMFs in bone repair.