Synthesis of new 4-aryloxy-N-arylanilines and their inhibitory activities against succinate-cytochrome c reductase.

Succinate-cytochrome c reductase (SCR) is composed of a mixture of mitochondrial complex II (succinate-ubiquinone oxidoreductase) and complex III (cytochrome bc1 complex). Meanwhile, complexes II and III are two promising targets of numerous antibiotics and fungicides. With an aim to identify new lead structures for SCR, complex II or III, a new series of 4-aryloxy-N-arylanilines were synthesized by introducing a 4-aryloxy phenyl group as one of the aryl groups in diaryl amines. With the economic Cu(OAc)2·H2O as the optimal copper promoter, a simple and facile protocol was utilized to afford 24 target products in 56-93% yields. Furthermore, extensive screening results suggested variable inhibitory activities of these compounds against SCR. Exceptionally, compounds 7k-7n showed excellent inhibition potency with their IC50 values in the nanomolar range, demonstrating higher potency than the commercial controls (penthiopyrad and azoxystrobin) by over one order of magnitude.

Ponicidin Treatment Improved the Cell Proliferation, Differentiation, and Calcium Mineralization on the Osteoblast-Like MG-63 Cells.

Osteoporosis is a general bone-related ailment characterized by reduced bone density and quality, elevated bone fragility, and fractures. It was reported that both aged men and women has an increased risks of osteoporosis. The current research work focused to unveil the beneficial roles of ponicidin treatment in the proliferation and calcium deposition on the osteoblast-like MG-63 cells. The effect of 5 and 10 µg/ml of ponicidin on the cell proliferation was assessed. The viability of ponicidin-supplemented MG-63 cells was inspected by MTT test. The contents of osteocalcin, collagen, and ALP activity in the ponicidin administered cells were assessed by kits. The level of calcium mineralization was examined by ARS staining technique. The ponicidin treatment remarkably improved the proliferation of MG-63 cells. The ponicidin did not affect the MG-63 cells viability but promoted its viability 24- and 48-h treatment. The contents of osteocalcin, collagen, and ALP activity in the 5 and 10 µg/ml of ponicidin-supplemented MG-63 cells were found increased than the control cells. The ponicidin also increased the level of calcium deposition in MG-63 cells, which is assessed by ARS staining. In conclusion, it was clear that ponicidin improved the proliferation and calcium mineralization in a MG-63 cells. Therefore, it was clear that ponicidin has helpful roles on the new bone development as a hopeful therapeutic candidate to treat the bone-related disease like osteoporosis.

Exploring the role of neurogenic pathway-linked cholecystokinin release in remote preconditioning-induced cardioprotection.

PURPOSE: The current study explored the involvement of neurogenic pathway-linked cholecystokinin (CCK) release in RIP-induced cardioprotection in rats. METHODS: Male Wistar rats were subjected to four cycles of alternate episodes of ischemia and reperfusion (five min each) to induce RIP. Thereafter, the hearts were subjected to global ischemia and reperfusion ex vivo. The myocardial damage was assessed by quantifying the levels of heartspecific biochemicals i.e. LDH-1, CK-MB and cTnT. Apoptotic cell injury was assessed by measuring the levels of caspase-3 and Bcl-2. The levels of CCK were measured in the plasma following RIP. RESULTS: Exposure to RIP significantly increased the plasma levels of CCK and attenuated IR-induced myocardial injury. Administration of CCK antagonist, proglumide significantly attenuated RIP-induced cardioprotection. Administration of hexamethonium, a ganglion blocker, abolished RIP-induced increase in plasma CCK levels and cardioprotective effects. Exogenous delivery of CCK-8 restored the effects of RIP in hexamethonium treated animals. CONCLUSION: RIP activates the neurogenic pathway that may increase the plasma levels of CCK, which may act on the heart-localized CCK receptors to produce cardioprotection against I/R injury.

Data for the synthesis of new 4-aryloxy-N-arylanilines as potent succinate-cytochrome c reductase inhibitors.

In this data article, we have designed a simple and facile protocol for copper-mediated synthesis of new 4-aryloxy-N-arylanilines under mild reaction conditions. The general information and synthetic procedures of all the target compounds were provided, and they were fully characterized by Nuclear Magnetic Resonance (NMR, including 1H NMR and 13C NMR), melting point measurements, and High-Resolution Mass Spectroscopy (HRMS). Furthermore, the inhibitory activities of these compounds against succinate-cytochrome c reductase (SCR) were evaluated, and the methods and procedures of enzyme inhibition experiments were also recorded in this data article. This article is related to "Synthesis of new 4-aryloxy-N-arylanilines and their inhibitory activities against succinate-cytochrome c reductase" (Cheng et al., 2018) [1].

Identification of potential therapeutic target genes and mechanisms in head and neck squamous cell carcinoma by bioinformatics analysis.

The present study aimed to identify the potential target genes and underlying molecular mechanisms involved in head and neck squamous cell carcinoma (HNSCC) by bioinformatics analysis. Microarray data of a Gene Expression Omnibus series GSE6631 was downloaded from the Gene Expression Omnibus database, which was generated from paired samples of HNSCC and normal tissue from 22 patients, and was used to identify differentially expressed genes (DEGs). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed to investigate the functions of the identified DEGs. Furthermore, the protein-protein interaction (PPI) network of these DEGs was constructed using Cytoscape software. Between HNSCC and normal samples there was a difference in 419 DEGs, including 196 upregulated and 223 downregulated genes. The upregulated DEGs were mainly enriched in GO terms of cell adhesion, extracellular matrix (ECM) organization and collagen metabolic process, while the downregulated DEGs were mainly associated with epidermis development and epidermal cell differentiation. The DEGs were enriched in pathways such as ECM-receptor interaction, focal adhesion and drug metabolism. Fibronectin 1 (FN1), epidermal growth factor receptor (EGFR), collagen type I alpha 1 (COL1A1) and matrix metallopeptidase-9 (MMP-9) were hub nodes in the PPI network. These results suggested that cell adhesion and drug metabolism may be associated with HNSCC development, and genes such as FN1, EGFR, COL4A1 and MMP-9 may be potential therapeutic target genes in HNSCC.

Exploring the role of neurogenic pathway-linked cholecystokinin release in remote preconditioning-induced cardioprotection

Abstract Purpose: The current study explored the involvement of neurogenic pathway-linked cholecystokinin (CCK) release in RIP-induced cardioprotection in rats. Methods: Male Wistar rats were subjected to four cycles of alternate episodes of ischemia and reperfusion (five min each) to induce RIP. Thereafter, the hearts were subjected to global ischemia and reperfusion ex vivo. The myocardial damage was assessed by quantifying the levels of heartspecific biochemicals i.e. LDH-1, CK-MB and cTnT. Apoptotic cell injury was assessed by measuring the levels of caspase-3 and Bcl-2. The levels of CCK were measured in the plasma following RIP. Results: Exposure to RIP significantly increased the plasma levels of CCK and attenuated IR-induced myocardial injury. Administration of CCK antagonist, proglumide significantly attenuated RIP-induced cardioprotection. Administration of hexamethonium, a ganglion blocker, abolished RIP-induced increase in plasma CCK levels and cardioprotective effects. Exogenous delivery of CCK-8 restored the effects of RIP in hexamethonium treated animals. Conclusion: RIP activates the neurogenic pathway that may increase the plasma levels of CCK, which may act on the heart-localized CCK receptors to produce cardioprotection against I/R injury.

[Intubation treatment of acute laryngeal obstruction: a case report].

Acute laryngeal obstruction is one of the most common diseases in Department of ENT, and it can cause suffocation without prompt treatment. Methods by using Nasopharyngofiberoscope guided tracheal intubation treatment of a case of acute laryngeal obstruction patients in a timely manner. This method is well tolerated, less trauma, high success rate, in the shortest time to improve the patient's ventilation, for the next step of the treatment to win the time.