Magnetic Hydroxyapatite-Coated Iron-Chromium Microspheres for Dental Surface Polishing and Plaque Removal.

This research aimed to engineer magnetic hydroxyapatite-coated iron-chromium (HAp-FeCr) microspheres to enhance dental surface polishing and plaque elimination. Utilizing a tailored sol-gel approach, the HAp-FeCr microspheres were synthesized and exhaustively characterized via scanning electron microscopy, energy-dispersive X-ray spectroscopy, ζ-potential, X-ray diffractometry, and X-ray photoelectron spectroscopy methodologies. Key findings showcased that these microspheres retained their magnetic properties post-HAp coating, as evidenced by the magnetization curves. An innovative magnetic polishing system was developed, incorporating these microspheres and a 2000 rpm magnet. Comparative evaluations between traditional air-powder polishing and the proposed magnetic technique demonstrated the latter's superiority. Notably, the magnetic polishing led to a substantial reduction in dental plaque on the tooth surface, decreasing bacterial adhesion and early biofilm formation by Streptococcus gordonii and Lactobacillus acidophilus, where the most pronounced effects were observed in samples with elevated HAp content. A significant 60% reduction in dental plaque was achieved with the magnetic method relative to air-powder polishing. Furthermore, the HAp-FeCr microspheres' biocompatibility was verified through cytotoxicity tests and animal studies. In essence, the magnetic HAp-FeCr microspheres present a novel and efficient strategy for dental treatments, holding immense potential for improving oral health.

New strategy of personalized tissue regeneration: when autologous platelet concentrates encounter biomaterials.

Components in blood play an important role in wound healing and subsequent tissue regeneration processes. The fibrin matrix and various bioactive molecules work together to participate in this complex yet vital biological process. As a means of personalized medicine, autologous platelet concentrates have become an integral part of various tissue regeneration strategies. Here, we focus on how autologous platelet concentrates play a role in each stage of tissue healing, as well as how they work in conjunction with different types of biomaterials to participate in this process. In particular, we highlight the use of various biomaterials to protect, deliver and enhance these libraries of biomolecules, thereby overcoming the inherent disadvantages of autologous platelet concentrates and enabling them to function better in tissue regeneration.

The effect of the "Oral-Gut" axis on periodontitis in inflammatory bowel disease: A review of microbe and immune mechanism associations.

Periodontitis and inflammatory bowel diseases (IBD) are inflammatory diseases of the gastrointestinal tract that share common features of microbial-induced ecological dysregulation and host immune inflammatory response. The close relationship between periodontitis and IBD is characterized by a higher prevalence of IBD in patients with periodontitis and a higher prevalence and severity of periodontitis in patients with IBD, indicating that periodontitis and IBD are different from the traditional independent diseases and form an "Oral-Gut" axis between the two, which affect each other and thus form a vicious circle. However, the specific mechanisms leading to the association between the two are not fully understood. In this article, we describe the interconnection between periodontitis and IBD in terms of microbial pathogenesis and immune dysregulation, including the ectopic colonization of the gut by pathogenic bacteria associated with periodontitis that promotes inflammation in the gut by activating the host immune response, and the alteration of the oral microbiota due to IBD that affects the periodontal inflammatory response. Among the microbial factors, pathogenic bacteria such as Klebsiella, Porphyromonas gingivalis and Fusobacterium nucleatum may act as the microbial bridge between periodontitis and IBD, while among the immune mechanisms, Th17 cell responses and the secreted pro-inflammatory factors IL-1ß, IL-6 and TNF-α play a key role in the development of both diseases. This suggests that in future studies, we can look for targets in the "Oral-Gut" axis to control and intervene in periodontal inflammation by regulating periodontal or intestinal flora through immunological methods.

Gold nanoparticle decoration potentiate the antibacterial enhancement of TiO2 nanotubes via sonodynamic therapy against peri-implant infections.

Inflammatory damage from bacterial biofilms usually causes the failure of tooth implantation. A promising solution for this challenge is to use an implant surface with a long-term, in-depth and efficient antibacterial feature. In this study, we developed an ultrasound-enhanced antibacterial implant surface based on Au nanoparticle modified TiO2 nanotubes (AuNPs-TNTs). As an artificial tooth surface, films based on AuNPs-TNTs showed excellent biocompatibility. Importantly, compared to bare titania surface, a larger amount of reactive oxygen radicals was generated on AuNPs-TNTs under an ultrasound treatment. For a proof-of-concept application, Porphyromonas gingivalis (P. gingivalis) was used as the model bacteria; the as-proposed AuNPs-TNTs exhibited significantly enhanced antibacterial activity under a simple ultrasound treatment. This antibacterial film offers a new way to design the surface of an artificial implant coating for resolving the bacterial infection induced failure of dental implants.

Asprosin in the Paraventricular Nucleus Induces Sympathetic Activation and Pressor Responses via cAMP-Dependent ROS Production.

Asprosin is a newly discovered adipokine that is involved in regulating metabolism. Sympathetic overactivity contributes to the pathogenesis of several cardiovascular diseases. The paraventricular nucleus (PVN) of the hypothalamus plays a crucial role in the regulation of sympathetic outflow and blood pressure. This study was designed to determine the roles and underlying mechanisms of asprosin in the PVN in regulating sympathetic outflow and blood pressure. Experiments were carried out in male adult SD rats under anesthesia. Renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP), and heart rate (HR) were recorded, and PVN microinjections were performed bilaterally. Asprosin mRNA and protein expressions were high in the PVN. The high asprosin expression in the PVN was involved in both the parvocellular and magnocellular regions according to immunohistochemical analysis. Microinjection of asprosin into the PVN produced dose-related increases in RSNA, MAP, and HR, which were abolished by superoxide scavenger tempol, antioxidant N-acetylcysteine (NAC), and NADPH oxidase inhibitor apocynin. The asprosin promoted superoxide production and increased NADPH oxidase activity in the PVN. Furthermore, it increased the cAMP level, adenylyl cyclase (AC) activity, and protein kinase A (PKA) activity in the PVN. The roles of asprosin in increasing RSNA, MAP, and HR were prevented by pretreatment with AC inhibitor SQ22536 or PKA inhibitor H89 in the PVN. Microinjection of cAMP analog db-cAMP into the PVN played similar roles with asprosin in increasing the RSNA, MAP, and HR, but failed to further augment the effects of asprosin. Pretreatment with PVN microinjection of SQ22536 or H89 abolished the roles of asprosin in increasing superoxide production and NADPH oxidase activity in the PVN. These results indicated that asprosin in the PVN increased the sympathetic outflow, blood pressure, and heart rate via cAMP-PKA signaling-mediated NADPH oxidase activation and the subsequent superoxide production.

Gut microbiota-dependent trimethylamine n-oxide pathway contributes to the bidirectional relationship between intestinal inflammation and periodontitis.

Background: Intestinal inflammation and periodontitis influence the development of each other through the bidirectional relationship. As the intestinal microbiome metabolite, trimethylamine-N-oxide (TMAO) could contribute to chronic inflammation in the gut by influencing the gut microbial composition and intestinal immunity. Increased circulating TMAO levels often accompany clinical findings in patients with experimental periodontitis. However, the role of TMAO in the bidirectional relationship between intestinal inflammation and periodontitis remains unclear. Thus, we explored whether TMAO influences the periodontitis process by affecting intestinal immunity and microbial composition in this article. Methods: Periodontitis was induced by unilateral ligation of the first molar in mice, and 3,3-dimethyl-1-butanol (DMB) was used as an inhibitor to reduce TMAO circulating. Twenty-five BALB/c mice were randomly assigned to five study sets (n = 5/group): no periodontitis with DMB (Control group), periodontitis (P) group, periodontitis with TMAO (P+TMAO) group, periodontitis with TMAO and DMB (P+TMAO+DMB) group, and periodontitis with DMB (P+DMB) group. The effect of TMAO was determined by assessing changes in intestinal histology, intestinal flora composition, periodontal tissue, and periodontal pro-inflammatory factors at ten days. Results: The outcomes indicated a marked improvement in the intestinal inflammation severity, and intestinal flora diversity was reduced. Firmicutes number and the ratio of Firmicutes/Bacteroidetes were improved in the P+TMAO group. In addition, the alveolar bone resorption and the degree of periodontal tissue inflammation were more severe in the P+TMAO group than in other groups. Immunohistochemistry showed higher levels of TGF-ß and IL-1ß expression in the periodontal tissues of P+TMAO. Conclusions: Our data suggest that TMAO could influence periodontal immunity and promote periodontal inflammation by affecting the intestinal microenvironment, revealing TMAO may affect the development of periodontitis through the bidirectional relationship of the oral-gut axis.

The protective effects of trelagliptin on high-fat diet-induced nonalcoholic fatty liver disease in mice.

Nonalcoholic fatty liver disease (NAFLD) occurs in patients with type 2 diabetes mellitus (T2DM). Trelagliptin is an important member of the Gliptins family, which has been recently licensed for the treatment of T2DM. However, the pharmacological function of trelagliptin in NAFLD has not been previously reported. In this study, we aimed to investigate the roles of trelagliptin in the development of NAFLD in a mouse model. To induce NAFLD disease, C57BL/6 mice were fed a high-fat diet for 10 weeks. Our results indicate that trelagliptin reduced plasma lipid levels in NAFLD mice by reducing triglycerides, total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol. Treatment with trelagliptin exhibited an improvement in insulin resistance. More important, trelagliptin improved liver function by reducing alanine transaminase, aspartate transaminase, lactate dehydrogenase, and total bile acid. In addition, trelagliptin ameliorated oxidative stress in the liver of NAFLD mice by reducing malondialdehyde and increasing the levels of reduced glutathione and superoxide dismutase activity. Also, the enzyme-linked immunosorbent assay results indicate that trelagliptin-treated mice displayed anti-inflammatory properties by reducing the levels of interleukin 1ß (IL-1ß), IL-6, and tumor necrosis factor-α. Hematoxylin and eosin and Oil red O staining show that trelagliptin treatment ameliorates liver tissue damage and hepatic lipid deposition. Mechanistically, we found that the administration of trelagliptin reduced the activity of hepatic nuclear factor-κB but increased the activity of AMP-activated protein kinase. These findings suggest that trelagliptin might become a promising therapeutic agent for the treatment of NAFLD.

Current Trends on Repurposing and Pharmacological Enhancement of Andrographolide.

Andrographolide, the main bioactive component separated from Andrographis paniculata in 1951, has been scrutinized with a modern drug discovery approach for anti-inflammatory properties since 1984. Identification of new uses of existing drugs can be facilitated by searching for evidence linking them to known or yet undiscovered drug targets and human disease states to develop new therapeutic indications.Furthermore, a wide spectrum of biological properties of andrographolide such as anticancer, antibacterial, antiviral, hepatoprotective, antioxidant, anti-malarial, anti-atherosclerosis are also reported. However, poor water solubility and instability limit its clinical application. It becomes crucial to enhance its pharmacological function and find a new treatment option for more diseases. Therefore, this article reviews the major recent developments in andrographolide, including repurposing applications in different diseases and underlying mechanisms, particularly focusing on pharmacological enhancement of andrographolide such as derivatives, chemical modifications with potent biological activity and drug delivery. The repurposing and pharmacological enhancement of andrographolide would not only have exciting therapeutic potential to different diseases to facilitate drug marketing, but also decrease the economic burden on healthcare worldwide.

The Inhibitory Effects of Juglanin on Adipogenesis in 3T3-L1 Adipocytes.

INTRODUCTION: Deregulation of adipogenesis plays an important role in obesity and other metabolism disorders. PPAR, C/EBP and SREBP1c are key transcriptional factors involved in adipogenesis and lipogenesis. Juglanin is a natural compound belonging to flavonoids, and it has been reported that juglanin has a potent inhibitory effect on inflammation and certain type of cancers. However, the effects of juglanin in adipogenesis have not been reported before. MATERIALS AND METHODS: 3T3-L1 preadipocytes were incubated with differentiation induction medium in the presence or absence of 0.5, 2.5, or 5 µM juglanin for an 8-day differentiation period. The lipid droplets accumulated in the cytoplasm were monitored by Oil Red O staining on days 0, 2, 5, and 8. The regulatory effects of juglanin on adipogenesis-related genes and proteins were investigated by real-time polymerase chain reaction and Western blot analysis. RESULTS: Juglanin significantly decreased lipid accumulation in differentiated adipocytes. Our findings show that juglanin reduced the expression of C/EBPα, C/EBPß, and SREBP-1c without affecting PPARα or PPARγ expression. Additionally, juglanin increased the activation of the SIRT1/AMPK signaling pathway through the phosphorylation of AMPKα. Finally, we performed an AMPK inhibitor experiment, which revealed that the inhibitory effects of juglanin on adipogenesis are mediated through AMPK. DISCUSSION: Juglanin can prevent adipogenesis by suppressing lipid accumulation and the differentiation of preadipocytes. The mechanism of juglanin regulating adipogenesis requires further investigation. Future clinical study in vivo could shed more light on its implication in modulating obesity and metabolic disorders.

Microporous Frameworks as Promising Platforms for Antibacterial Strategies Against Oral Diseases.

Nowadays, the heavy burden of oral diseases such as dental caries, periodontitis, endodontic infections, etc., and their consequences on the patients' quality of life indicate a strong need for developing effective therapies. Bacterial infections played an important role in the field of oral diseases, in-depth insight of such oral diseases have given rise to the demand for antibacterial therapeutic strategies. Recently, microporous frameworks have attracted tremendous interest in antibacterial application due to their well-defined porous structures for drug delivery. In addition, intensive efforts have been made to enhance the antibacterial performance of microporous frameworks, such as ion doping, photosensitizer incorporation as building blocks, and surface modifications. This review article aims on the major recent developments of microporous frameworks for antibacterial applications against oral diseases. The first part of this paper puts concentration on the cutting-edge researches on the versatile antibacterial strategies of microporous materials via drug delivery, inherent activity, and structural modification. The second part discusses the antibacterial applications of microporous frameworks against oral diseases. The applications of microporous frameworks not only have promising therapeutic potential to inhibit bacterial plaque-initiated oral infectious diseases, but also have a wide applicability to other biomedical applications.

BMP-2-Loaded HAp:Ln3+ (Ln = Yb, Er, Gd) Nanorods with Dual-Mode Imaging for Efficient MC3t3-E1 Cell Differentiation Regulation.

Effective bone tissue reconstitution improves the treatment success rate of dental implantation and preserves natural teeth during periodontal tissue repair. Hydroxyapatite (HAp) has received much attention in bone remodeling field because its mineralized structure is similar to that of the natural bone tissue. For this reason, it has been used as a carrier for growth factors. Although HAp possesses outstanding biomedical properties, its capacity of loading and releasing bone growth factors and promoting osteogenesis is not well understood. In this study, Ln3+ (Ln = Yb3+, Er3+, Gd3+)-doped HAp (HAp:Ln3+) nanorods were synthesized by one-step hydrothermal method. To improve its biocompatibility and surface properties, bone morphogenetic protein-2 (BMP-2) was loaded onto the surface of HAp:Ln3+ nanorods. The results showed that BMP-2 incorporation promoted bone formation and enhanced the expression of early bone-related gene and protein (RunX2, SP7, OPN). In addition, Yb3+- and Er3+-doped HAp nanorods were examined by upconversion luminescence with 980 nm near-infrared laser irradiation to monitor the delivery position of BMP-2 protein. Furthermore, due to the positive magnetism correlated with the concentration of Gd3+, HAp:Ln3+ with enhanced contrast brightening can be deemed as T1 MIR contrast agents. These findings indicate that HAp doped with rare-earth ions and loaded with BMP-2 has the potential to promote bone tissue repair and execute dual-mode imaging.

Protective effect of ginsenoside Rg3 on lung injury in diabetic rats.

Ginsenoside has been used to treat diabetes, while ginsenoside Rg3 is the main active ingredient component of ginseng and is used to study its effects on lung tissue damage in diabetic rats. In this paper, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry were applied to detect the proliferation and apoptosis of BEAS-2B cells treated with different concentrations of Rg3. The inflammatory response and pathological change in the lung tissue of diabetic rats treated with Rg3 were evaluated by enzyme-linked immunosorbent assay, quantative real-time polymerase chain reaction, and hematoxylin and eosin staining immunohistochemistry. Meanwhile, PI3K and MAPK signaling pathway proteins in lung tissue were determined by Western blot analysis. The results showed that ginsenoside Rg3 had no significant influence on the proliferation and apoptosis of BEAS-2B cells. Ginsenoside Rg3 can inhibit inflammatory response and promote the activation of PI3K and MAPK signaling pathways to prevent damages of lung tissues induced by hyperglycemia. The protective effect provided by ginsenoside Rg3 indicates that ginsenoside Rg3 is a potential drug for the treatment of diabetes.

The Resveratrol Alleviates the Hepatic Toxicity of CuSO4 in the Rat.

Cu is toxic to humans and other animals. Oxidative stress is an important mechanism involved in Cu toxicity. Resveratrol (RSV) is an antioxidative compound, so could counteract Cu toxicity. The aim of this study was to determine whether RSV protects the liver from the effects of CuSO4. Forty male Sprague-Dawley rats (5 weeks old, 110-120 g) were divided into four groups (n = 10 per group), a control group and groups treated with CuSO4 at a dose of 200 mg/kg body weight (BW), RSV at a dose of 15 mg/kg BW, and CuSO4 at a dose of 200 mg/kg BW and RSV at a dose of 15 mg/kg BW. The treatments were orally administered for 30 days. The livers were removed from the rats at the end of the study, and the cytochrome P450, cytochrome b5, Cu, Fe, Zn, glutathione peroxidase, superoxide dismutase, reactive oxygen species, aspartate aminotransferase, and alanine aminotransferase concentrations in the livers were determined. CuSO4 decreased the BW, liver weight, and cytochrome P450, cytochrome b5, Fe, Zn, glutathione peroxidase, and superoxide dismutase concentrations but increased the Cu, aspartate aminotransferase, alanine aminotransferase, and reactive oxygen species concentrations relative to the control group. RSV alleviated the toxic effects of CuSO4 on the liver, indicating that RSV attenuates CuSO4-induced liver injury by decreasing the liver transaminase concentration and oxidative stress, promoting antioxidative activity and cytochrome P450 enzymes, and maintaining balance in the trace element concentrations. The results indicate that RSV could be used to treat CuSO4 toxicity.

Surface functionalization of TiO2 nanotubes with minocycline and its in vitro biological effects on Schwann cells.

BACKGROUND: Minocycline has been widely used in central nervous system disease. However, the effect of minocycline on the repairing of nerve fibers around dental implants had not been previously investigated. The aim of the present study was to evaluate the possibility of using minocycline for the repairing of nerve fibers around dental implants by investigating the effect of minocycline on the proliferation of Schwann cells and secretion of neurotrophic factors nerve growth factor and glial cell line-derived neurotrophic factor in vitro. METHODS: TiO2 nanotubes were fabricated on the surface of pure titanium via anodization at the voltage of 20, 30, 40 and 50 V. The nanotubes structure were characterized by scanning electron microscopy and examined with an optical contact angle. Then drug loading capability and release behavior were detected in vitro. The TiO2 nanotubes loaded with different concentration of minocycline were used to produce conditioned media with which to treat the Schwann cells. A cell counting kit-8 assay and cell viability were both selected to study the proliferative effect of the specimens on Schwann cell. Reverse transcription-quantitative PCR and western blot analyses were used to detect the related gene/protein expression of Schwann cells. RESULTS: The results showed that the diameter of TiO2 nanotubes at different voltage varied from 100 to 200 nm. The results of optical contact angle and releasing profile showed the nanotubes fabricated at the voltage of 30 V met the needs of the carrier of minocycline. In addition, the TiO2 nanotubes loaded with the concentration of 20 µg/mL minocycline increased Schwann cells proliferation and secretion of neurotrophic factors in vitro. CONCLUSIONS: The results suggested that the surface functionalization of TiO2 nanotubes with minocycline was a promising candidate biomaterial for the peripheral nerve regeneration around dental implants and has potential to be applied in improving the osseoperception of dental implant.