GLUT1 Promotes NLRP3 Inflammasome Activation of Airway Epithelium in Lipopolysaccharide-Induced Acute Lung Injury.

Acute lung injury (ALI) is a devastating clinical syndrome caused by different factors, with high morbidity and mortality. Lung injury and inflammation caused by lipopolysaccharide (LPS) can be modulated by NLRP3 inflammasome activation, yet its exact function within the airway epithelium is still unknown. Meanwhile, glucose transporter protein 1 (GLUT1) contributes to a number of inflammatory illnesses, including ALI. The present study aimed to assess GLUT1's function in NLRP3 inflammasome activation of airway epithelium in LPS-induced acute lung injury. BALB/c mice and BEAS-2B cells were exposed to LPS (5 mg/kg and 200 µg/mL, respectively), with or without GLUT1 antagonists (WZB117 or BAY876). LPS up-regulated pulmonary expression of NLRP3 and GLUT1 in mice, which could be blocked by WZB117 or BAY876. Pharmacological inhibition of GLUT1 in vivo significantly attenuated lung tissue damage, neutrophil accumulation, and proinflammatory factors release (TNF-α, IL-6, and IL-1ß) in LPS-exposed mice. Meanwhile, the activation markers of NLRP3 inflammasome (ASC, caspase-1, IL-1ß, and IL-18) induced by LPS were also suppressed. In cultured BEAS-2B cells, LPS induced an increase in GLUT1 expression and triggered activation of the NLRP3 inflammasome, both of which were inhibited by GLUT1 antagonists. These results illustrate that GLUT1 participates in LPS-induced ALI and promotes the activation of the NLRP3 inflammasome in airway epithelial cells.

GLUT1 regulates the release of VEGF-A in the alveolar epithelium of lipopolysaccharide-induced acute lung injury.

Acute lung injury (ALI) is a severe disease with high mortality and poor prognosis, characterized by excessive and uncontrolled inflammatory response. Vascular endothelial growth factor A (VEGF-A) contributes to the development and progression of ALI. The aim of this study was to evaluate the role of glucose transporter 1 (GLUT1) in alveolar epithelial VEGF-A production in lipopolysaccharide (LPS)-induced ALI. An ALI mouse model was induced by LPS oropharyngeal instillation. Mice were challenged with LPS and then treated with WZB117, a specific antagonist of GLUT1. For the vitro experiments, cultured A549 cells (airway epithelial cell line) were exposed to LPS, with or without the GLUT1 inhibitors WZB117 or BAY876. LPS significantly upregulated of GLUT1 and VEGF-A both in the lung from ALI mice and in cultured A549. In vivo, treatment with WZB117 not only markedly decreased LPS-induced pulmonary edema, injury, neutrophilia, as well as levels of interleukin (IL)-1ß, IL-6 and tumor necrosis factor-α in bronchoalveolar lavage fluid (BALF), but also reduced VEGF-A production. Yet, the maximum tolerated concentration of WZB117 failed to suppress LPS-induced VEGF-A overexpression in vitro. While administration of BAY876 inhibited gene and protein expression as well as secretion of VEGF-A in response to LPS in A549. These results illustrated that GLUT1 upregulates VEGF-A production in alveolar epithelia from LPS-induced ALI, and inhibition of GLUT1 alleviates ALI.

Achieving Luminescence of Sr3Ga1.98In0.02Ge4O14:0.03Cr3+ via [In3+] Substitution [Ga3+] and Its Application to NIR pc-LED in Non-Destructive Testing.

Cr3+-doped Sr3Ga2Ge4O14:0.03Cr3+ (SGGO:0.03Cr3+) phosphor was synthesized via a high-temperature solid-phase method. Considering the tunable structure of SGGO, Ga3+ ions in the matrix were substituted with In3+ ions at a certain concentration. The tuned phosphor produced a red-shifted emission spectrum, with its luminescence intensity at 423 K maintained at 63% of that at room temperature; moreover, the internal quantum efficiency increased to 65.60%, and the external quantum efficiency correspondingly increased to 21.94%. On this basis, SGIGO:0.03Cr3+ was encapsulated into a pc-LED, which was applied in non-destructive testing (NDT) experiments, successfully realizing the recognition of water and anhydrous ethanol, proving its potential application in the field of NDT.

IRE1α/XBP-1 promotes ß-catenin signaling activation of airway epithelium in lipopolysaccharide-induced acute lung injury.

BACKGROUND: Acute lung injury (ALI), along with the more severe condition--acute respiratory distress syndrome (ARDS), is a major cause of respiratory failure in critically ill patients with high morbidity and mortality. Inositol-requiring protein 1α (IRE1α)/X box protein-1 (XBP1) pathway was proved to regulate lipopolysaccharide (LPS)-induced lung injury and inflammation. Yet, its role on epithelial ß-catenin in LPS-induced ALI remains to be elucidated. METHODS: LPS-induced models were generated in mice (5 mg/kg) and Beas-2B cells (200 µg/mL). Two selective antagonists of IRE1α (4µ8c and STF-083010) were respectively given to LPS-exposed mice and cultured cells. RESULTS: Up-regulated expression of endoplasmic reticulum (ER) stress markers immunoglobulin-binding protein (BIP) and spliced X box protein-1(XBP-1s) was detected after LPS exposure. Besides, LPS also led to a down-regulated total ß-catenin level in the lung and Beas-2B cells, with decreased membrane distribution as well as increased cytoplasmic and nuclear accumulation, paralleled by extensively up-regulated downstream targets of the Wnt/ß-catenin signaling. Treatment with either 4µ8c or STF-083010 not only significantly attenuated LPS-induced lung injury and inflammation, but also recovered ß-catenin expression in airway epithelia, preserving the adhesive function of ß-catenin while blunting its signaling activity. CONCLUSION: These results illustrated that IRE1α/XBP1 pathway promoted the activation of airway epithelial ß-catenin signaling in LPS-induced ALI.

Efficient near-infrared broadband garnet phosphor for pc-LED and its application to vascular visualization and night vision.

Ultra-broadband near-infrared (NIR) spectroscopy has unparalleled application prospects in intelligent detection and phosphor-converted light-emitting diodes (pc-LED), which are most likely to become the next generation of NIR light sources, has become a hot spot for research nowadays. To cope with the demand for more NIR spectroscopy applications, more efficient NIR phosphors need to be developed. Here, by screening the subject with a smaller band gap and by screening the suitable ion electronegativity of the lattice position where the Cr3+ is located, and then through the energy transfer, a series of Gd3Zn2GaGe2O12:xCr3+, yYb3+ (GZGG:Cr3+/Yb3+) NIR broadband garnet phosphors were found for the first time. By controlling the energy transfer process, the internal quantum yield (IQY) (54.9%), external quantum yield (EQY) (24.65%), bandwidth (260 nm), and thermal stability (60% at 150 °C) of NIR emission were substantially improved. The obtained phosphors are packaged with blue light chips into pc-LED, which can be applied in different fields such as vascular visualization and night vision.

Near-Infrared Broadband ZnTa2O6:Cr3+ Phosphor for pc-LEDs and Its Application to Nondestructive Testing.

Broadband near-infrared (NIR) phosphors are necessary materials for developing portable NIR light sources. Moreover, exploiting an NIR phosphor with a main peak located beyond a wavelength of 900 nm remains a challenge because this spectral range has great potential in biological nondestructive testing and solution testing. In this study, a range of Cr3+-doped ZnTa2O6 (ZTO) phosphors were completely synthesized by a solid-state method, which show broadband Cr3+ emission centered at 935 nm with a large full width at half maximum (FWHM) of 185 nm due to two distorted octahedral sites. A packaged phosphor-converted light-emitting diode (pc-LED) device is used to penetrate a 5-cm-thick chicken breast and identify diverse solutions based on differences in the measured transmission spectra. The results indicate broad application prospects in the field of biological tissue penetration and solution analysis.

Chromium(III)-Doped Phosphors of High-Efficiency Two-Site Occupation Broadband Infrared Emission for Vessel Visualization Applications.

The exploration of efficient broadband near-infrared (NIR) emitting materials is essential to establishing new NIR applications. In this work, an excellent NIR phosphor Mg7Ga2GeO12:Cr3+, with an emission band of 650-1350 nm and a full width at half maximum of 266 nm, was successfully prepared. When Ga3+ ions were replaced by In3+ ions, its emission intensity increased 4 times, and the internal and external quantum efficiency reached 86 and 37%, respectively. A NIR phosphor-converted light-emitting diode (pc-LED) component was made by combining a synthetic Mg7Ga1.84In0.07GeO12:0.09Cr3+ phosphor with a 450 nm blue luminescent chip. The vascular and skeletal distribution on human fingers and the back of the hand can be seen under the display of a commercial NIR camera, indicating that Mg7Ga1.84In0.07GeO12:0.09Cr3+ phosphors have promising applications in the field of the blood vessel and bone visualization.

Ultra-sensitive luminescence ratiometric thermometry from 2E→4A2 transitions of AlTaO4:Cr3.

In recent years, non-contact ratiometric luminescence thermometry has continued to gain popularity among researchers, owing to its compelling features, such as high accuracy, fast response, and convenience. The development of novel optical thermometry with ultrahigh relative sensitivity (Sr) and temperature resolution has become a frontier topic. In this work, we present a novel, to the best of our knowldege, luminescence intensity ratio (LIR) thermometry method that relies on AlTaO4:Cr3+ materials, based on the fact that they possess both anti-Stokes phonon sideband emission and R-line emission at the 2E→4A2 transitions and have been confirmed to follow the Boltzmann distribution. In the temperature range 40-250 K, the emission band of the anti-Stokes phonon sideband shows an upward trend, while the bands of the R-lines show the opposite downward trend. Relying on this fascinating feature, the newly proposed LIR thermometry achieves a maximum relative sensitivity of 8.45%K-1 and a temperature resolution of 0.038 K. Our work is expected to provide guiding insights for optimizing the sensitivity of Cr3+-based LIR thermometers and provide some novel entry points for designing excellent and reliable optical thermometers.

Two novel resin glycosides isolated from Ipomoea cairica with α-glucosidase inhibitory activity.

In the present study, two new compounds from Ipomoea cairica were identified and demonstrated to have α-glucosidase inhibitory activity. They were isolated by column chromatography on silica gel and sephadex LH-20 and finally purified by prep-HPLC, with their structures being elucidated by spectroscopic methods, such as 1D- and 2D-NMR and HR-TOF-MS, and chemical methods. Compounds 1 and 2, named cairicoside A and cairicoside B, were evaluated for α-glucosidase inhibitory activity by the MTT method, with the IC50 values being 25.3 ± 1.6 and 28.5 ± 3.3 µmol·L(-1), respectively.

Four new pentasaccharide resin glycosides from Ipomoea cairica with strong α-glucosidase inhibitory activity.

Six pentasaccharide resin glycosides from Ipomoea cairica, including four new acylated pentasaccharide resin glycosides, namely cairicoside I-IV (1-4) and the two known compounds cairicoside A (5) and cairicoside C (6), were isolated from the aerial parts of Ipomoea cairica. Their structures were established by a combination of spectroscopic, including two dimensional (2D) NMR and chemical methods. The core of the six compounds was simonic acid A, and they were esterfied the same sites, just differing in the substituent groups. The lactonization site of the aglycone was bonded to the second saccharide moiety at C-2 in 1-4, and at C-3 in 5-6. Compounds 1 and 5, 4 and 6 were two pairs of isomers. The absolute configuration of the aglycone in 1-6 which was (11S)-hydroxyhexadecanoic acid (jalapinolic acid) was established by Mosher's method. Compounds 1-4 have been evaluated for inhibitory activity against α-glucosidase, which all showed inhibitory activities.

Diaqua-bis-(3-nitro-benzoato-κO)bis-[1H-5-(3-pyrid-yl)-3-(4-pyrid-yl)-1H-1,2,4-triazole-κN]cobalt(II) dihydrate.

In the centrosymmetric title compound, [Co(C(7)H(4)NO(4))(2)(C(12)H(9)N(5))(2)(H(2)O)(2)]·2H(2)O, the Co(II) atom, located on an inversion center, is coordinated by two N atoms [Co-N = 2.155 (3) Å] and four O atoms [Co-O = 2.099 (2)-2.117 (3) Å] in a distorted octa-hedral geometry. Inter-molecular N-H⋯O, O-H⋯N and O-H⋯O hydrogen bonds link the components into a three-dimensional supramolecular framework.