Long-term poor glycemic control negatively affects macrovascular and microvascular diseases, as well as wound restoration. Buckwheat is a good source of rutin (quercetin-3-O-rutoside) and has benefits in regulating blood sugar. This study was to evaluate the antioxidant and anti-inflammatory effects of rutin on wound healing in streptozotocin-induced hyperglycemic rats. Eighteen male Wistar rats were randomly divided into three groups: normal (NDM), hyperglycemic (DM), and hyperglycemic with rutin (DMR). After induction of hyperglycemia for 2 days, a 15 × 15 mm wound was induced on the back of each rat. Intraperitoneal injection of rutin significantly ameliorated diabetes-induced body weight loss and improved metabolic dysfunctions of hyperglycemic rats. Based on appearance and histopathological staining, rutin promotes wound healing and inhibits production of inflammatory cells. The immunoblotting data indicated that rutin promotes production of antioxidant enzymes induced by nuclear factor erythroid 2-related factor 2 (NRF2), inhibits the expression of matrix metalloproteinases (MMPs) regulated by NF-κB, and decreases the expression of vascular endothelial growth factor (VEGF). It also promotes the expression of neurogenic-related protein (UCH-L1). The aforementioned results indicated that rutin reduces oxidative stress and inflammatory response in hyperglycemic rats, promoting wound healing and subsequently reducing the risk of wound ulcers.

In this study, five urethane acrylates (UAs), namely aliphatic urethane hexa-acrylate (87A), aromatic urethane hexa-acrylate (88A), aliphatic UA (588), aliphatic urethane triacrylate diluted in 15% HDD (594), and high-functional aliphatic UA (5812), were selected to formulate five UA-based photopolymer resins for digital light processing (DLP)-based 3D printing. Each UA (40 wt%) was added and blended homogenously with ethoxylated pentaerythritol tetraacrylate (40 wt%), isobornyl acrylate (12 wt%), diphenyl (2,4,6-trimethylbenzoyl) phosphine oxide (3 wt%), and a pink acrylic (5 wt%). Each UA-based resin specimen was designed using CAD software and fabricated using a DLP 3D printer to specific dimensions. Characteristics, mechanical properties, and cytotoxicity levels of these designed UA-based resins were investigated and compared with a commercial 3D printing denture base acrylic resin (BB base) control group at different UV exposure times. Shore hardness-measurement data and MTT assays were analyzed using a one-way analysis of variance with Bonferroni’s post hoc test, whereas viscosity, maximum strength, and modulus were analyzed using the Kruskal–Wallis test (α = 0.05). UA-based photopolymer resins with tunable mechanical properties were successfully prepared by replacing the UA materials and the UV exposure times. After 15 min of UV exposure, the 5812 and 594 groups exhibited higher viscosities, whereas the 88A and 87A groups exhibited lower viscosities compared with the BB base group. Maximum flexural strength, flexural modulus, and Shore hardness values also revealed significant differences among materials (p < 0.001). Based on MTT assay results, the UA-based photopolymer resins were nontoxic. In the present study, mechanical properties of the designed photopolymer resins could be adjusted by changing the UA or UV exposure time, suggesting that aliphatic urethane acrylate has good potential for use in the design of printable resins for DLP-type 3D printing in dental applications.

Early-life sleep deprivation (ESD) is a serious condition with severe cognitive sequelae. Considering hippocampus plays an essential role in cognitive regulation, the present study aims to determine whether melatonin, a neuroendocrine beard with significant anti-oxidative activity, would greatly depress the hippocampal oxidative stress, improves the molecular machinery, and consequently exerts the neuro-protective effects following ESD. Male weanling Wistar rats (postnatal day 21) were subjected to ESD for three weeks. During this period, the animals were administered normal saline or melatonin (10 mg/kg) via intraperitoneal injection between 09:00 and 09:30 daily. After three cycles of ESD, the animals were kept under normal sleep/wake cycle until they reached adulthood and were sacrificed. The results indicated that ESD causes long-term effects, such as impairment of ionic distribution, interruption of the expressions of neurotransmitters and receptors, decreases in the levels of several antioxidant enzymes, and impairment of several signaling pathways, which contribute to neuronal death in hippocampal regions. Melatonin administration during ESD prevented these effects. Quantitative evaluation of cells also revealed a higher number of neurons in the melatonin-treated animals when compared with the saline-treated animals. As the hippocampus is critical to cognitive activity, preserving or even improving the hippocampal molecular machinery by melatonin during ESD not only helps us to better understand the underlying mechanisms of ESD-induced neuronal dysfunction, but also the therapeutic use of melatonin to counteract ESD-induced neuronal deficiency.

Excessive exposure to club drug (GHB) would cause cognitive dysfunction in which impaired hippocampal Ca²⁺-mediated neuroplasticity may correlate with this deficiency. However, the potential changes of in vivo Ca²⁺ together with molecular machinery engaged in GHB-induced cognitive dysfunction has never been reported. This study aims to determine these changes in bio-energetic level through ionic imaging, spectrometric, biochemical, morphological, as well as behavioral approaches. Adolescent rats subjected to GHB were processed for TOF-SIMS, immunohistochemistry, biochemical assay, together with Morris water maze to detect the ionic, molecular, neurochemical and behavioral changes of GHB-induced cognitive dysfunction, respectively. Extent of oxidative stress and bio-energetics were assessed by levels of lipid peroxidation, Na⁺/K⁺ ATPase, cytochrome oxidase and [¹⁴C]-2-deoxyglucose activity. Results indicated that in GHB intoxicated rats, decreased Ca²⁺ imaging and reduced NMDAR1, nNOS and p-CREB reactivities were detected in hippocampus. Depressed Ca²⁺-mediated signaling corresponded well with intense oxidative stress, diminished Na⁺/K⁺ ATPase, reduced COX and decreased 2-DG activity, which all contributes to the development of cognitive deficiency. As impaired Ca²⁺-mediated signaling and oxidative stress significantly contribute to GHB-induced cognitive dysfunction, delivering agent(s) that improves hippocampal bio-energetics may thus serve as a promising strategy to counteract the club drug-induced cognitive dysfunction emerging in our society nowadays.