Search

Sepiella maindroni ink, a flavoring and coloring agent in food, has attracted considerable attention due to its various pharmacological activities. Our previous study showed that the melanin of Sepiella maindroni ink (MSMI) can alleviate oxidative damage and delay aging in D-galactose(D-gal)-induced aging mice. This study aimed to reveal the possible mechanisms of the anti-aging effect of MSMI. In this article, a comprehensive analysis of gas chromatography-mass spectrometry (GC-MS)-based metabolomics and microarray-based transcriptomics revealed that 221 mRNAs were differentially expressed and 46 metabolites were significantly changed in the anti-aging progress of MSMI. Integrated analysis of transcript and metabolic profiles indicated that MSMI mainly altered carbohydrate metabolism, lipid metabolism, and insulin signaling pathway. MSMI achieved anti-aging effects not only by reducing oxidative damage and sorbitol toxicity but also by regulating lipid metabolism, improving insulin sensitivity, and reducing the formation of advanced glycation end products (AGEs). Moreover, our findings firstly demonstrated that MSMI could increase the expression of interferon-induced proteins and might be a potential antiviral compound.

AimsCu, Pb and Cd are common heavy metals in mangroves. Objective to clone chitinase I gene in mangrove plants and explore the role of chitinase I gene in plants under heavy metal stress. MethodsHomologous cloning and RACE cloning were used to clone chitinase type I gene in mangrove plants, and bioinformatics analysis software was used to analyze and predict gene structure and functional domain. The mRNA expression pattern of chitinase gene in mangrove plants under heavy metal stress was analyzed by real-time quantitative PCR analysis. ResultsAll Four cDNA with a full length of 1092 bp, and an ORF (open reading frame) 831 bp, coding with 276 amino acids, while are differences in the sequences among the four species. Four genes owned signal peptide and were located at vacuole inside the cell. Protein sequence domain analysis indicates that all have the same typical structural characteristics of GH19 chitinase family. The sequence of CHI had high similarity to the protein sequences of Camellia fraternal chitinases. Real-time PCR was used to analyze the expression of CHI under different concentration heavy metal with time of four mangrove species. The gene expression of CHI I was highly induced in the B.gymnorrhiza leaves than other mangrove species. With the increase of heavy metal stress time, the expression level of B.gymnorrhiza increased continuously.ConclusionChitinase was induced under heavy metal in mangrove plants, and chitinase plays an active part in heavy metal tolerance in mangrove plants which was located at vacuole inside the cell.

A new iridium(III) complex Ir(tbt)2(fppz) (2) (fppzH = 2-(3-trifluoromethyl-1H-pyrazol-5-yl)-pyridine) with a triptycenylbenzothiazole (tbt) ligand and its parent complex Ir(bt)2(fppz) (1) with a phenylbenzothiazole (bt) ligand have been synthesized and characterized. The decomposition temperature (Td(5%)) of complex 2 is 395 °C, which is 16 °C higher than that of parent complex 1. Complex 2 showed an emission peak at 546 nm with a PLQY of 67.8%. When compared with complex 1, its luminescent wavelength red-shifted by 11 nm, the PLQY increased by 13% and the luminescent lifetime shortened by 20%. Moreover, the luminescence quenching of complex 2 at a high concentration (30 wt% in PMMA) is found to be effectively prevented, and the PLQY of complex 2 is three times more than that of complex 1. The electron-donating nature of the triptycene scaffold pushes up the HOMO level of complex 2. As a result, complex 2 achieves a higher non-doped device performance, revealing a maximum current efficiency/EQE of 12.6 cd A−1/5.5%, which are obviously higher than that of complex 1 (9.8 cd A−1, 3.8%). The doped device of complex 2 shows a maximum current efficiency/EQE of 29.8 cd A−1/11.8%. These findings suggest that the comprehensive performance of iridium(III) complexes can be obviously improved by the careful introduction of a triptycene scaffold.

It was studied for the effects of heavy metal stress on the antioxidant activities of superoxide dismutase (SOD), peroxidase (POD), catalase (CAT) and lipid peroxidation (MDA) in the leaves of five mangrove plants. The results showed the protein concentrations were significantly higher in B. gymnorrhiza (7.55 mg prot /mL: Cu2+), K. obovata (11.21 mg prot/mL: Cd2+) and R. stylosa (12.51 mg prot/mL: Cd2+) (p

A series of charge-neutral cyclometalated iridium(III) complexes (1–3 and 5–7) containing triptycene-substituted ligands (tbt and tpbi) and two parent complexes (4 and 8) were synthesized and characterized. The crystal structures indicated that π–π stacking interactions existed in ligand tbtH, but not in complex 6. However, a large intramolecular repulsion was found in complex 6. These triptycene-based complexes exhibited good thermal stability, which was higher compared with that of the parent complexes. These complexes showed green to yellow emission with peaks that ranged from 503 to 563 nm. The introduction of the rigid non-conjugate triptycene skeleton caused a slight emission red shift ( 47%) was observed. The electroluminescent devices employing 2 and 6 as phosphors displayed impressive performance improvements and low efficiency roll-off because of the higher PLQYs and HOMO levels of these triptycene-based complexes. The maximum current and external quantum efficiencies of the devices based on complexes 2 and 6 were 41.7 cd A−1, 11.9% and 41.2 cd A−1, 12.6%, respectively, which were about 31% higher than that of the devices based on the parent complexes 4 and 8. This work provides a novel approach to develop highly efficient phosphors with a triptycene skeleton.

Three novel highly efficient blue bicyclometalated iridium(III) complexes (Ir1–Ir3) were designed and synthesized with 4-(2, 6-difluoropyridin-3-yl)-6-mesitylpyrimidine as primary ligands. The alternation of ancillary ligands had precisely regulated their emitting peaks from sky-blue to deep-blue. These complexes exhibit unimodal emission with PLQYs higher than 90% and lifetimes shorter than 1.1 μs. These complexes also show good thermal stability with Td > 320 °C. The OLED using complex Ir3 as emitter in 13 wt% exhibited a maximum luminous efficiency of 16.9 cd A−1 with a high EQE of 13.0%. The CIE coordinates of this device are (0.15, 0.16), which are close to the standard blue color region.

Two one-pot methods have been used to synthesize various homoleptic phenylpyridazine iridium (III) complexes (2–4). The coordination arrangements of 2 and 3 were revealed by carrying out single X-ray structural analyses. These complexes showed green emission. Their peak wavelengths ranged from 508 to 538 nm with quantum yields greater than 70%. Density functional theory (DFT) was used to discuss the correlation between substituent nature and photophysical characteristics of these complexes. Organic light-emitting diodes (OLEDs) were fabricated by taking 2–4 as dopants. The green device based on complex 4 shows a maximum current efficiency and external quantum efficiency of 78.6 cd A−1 and 21.9%, respectively, and mild efficiency roll-off. The results suggest that these homoleptic phenylpyridazine iridium(III) complexes have potential application as efficient emitters in OLEDs.

Cartilage has limited repair and regeneration capacity, thus damage of cartilage often results in its dysfunction and even chronic diseases like osteoarthritis (OA). Chondrogenesis induced by tissue-engineering methods is essential to treating cartilage-related diseases. MicroRNAs (miRNAs) are a class of small non-coding single-stranded RNAs which exert their biological effects by binding to the target messenger RNAs (mRNAs), resulting in decay or translation suppression of target mRNAs. There are emerging evidence indicating that miRNAs may play important roles in regulating both prenatal and postnatal chondrogenesis. During embryonic skeletal development, prenatal chondrogenesis is thought to be a precondition for formation of cartilage in developing limbs. Plenty of studies on different types of stem cells have undoubtedly proven their capacity of differentiating into chondrocytes. MiRNAs are found to comprehensively modulate these processes by establishing an interaction network with target genes, transcription factors and cytokines et al. In addition, translational application of miRNA technology has also been explored. In this review, we focus on the up-dated progress on regulatory mechanisms of miRNAs in prenatal and postnatal chondrogenesis. In addition, several miRNA target genes and roles of miRNAs in cartilage-related diseases are also discussed. This will contribute to studies of chondrogenesis mechanisms and development of new treating methods.

Huntington's disease is an inherited and incurable neurodegenerative disorder caused by an abnormal polyglutamine (polyQ) expansion in huntingtin (encoded by HTT). PolyQ length determines disease onset and severity, with a longer expansion causing earlier onset. The mechanisms of mutant huntingtin-mediated neurotoxicity remain unclear; however, mitochondrial dysfunction is a key event in Huntington's disease pathogenesis. Here we tested whether mutant huntingtin impairs the mitochondrial fission-fusion balance and thereby causes neuronal injury. We show that mutant huntingtin triggers mitochondrial fragmentation in rat neurons and fibroblasts of individuals with Huntington's disease in vitro and in a mouse model of Huntington's disease in vivo before the presence of neurological deficits and huntingtin aggregates. Mutant huntingtin abnormally interacts with the mitochondrial fission GTPase dynamin-related protein-1 (DRP1) in mice and humans with Huntington's disease, which, in turn, stimulates its enzymatic activity. Mutant huntingtin-mediated mitochondrial fragmentation, defects in anterograde and retrograde mitochondrial transport and neuronal cell death are all rescued by reducing DRP1 GTPase activity with the dominant-negative DRP1 K38A mutant. Thus, DRP1 might represent a new therapeutic target to combat neurodegeneration in Huntington's disease.