Search

Two polypyridyl ruthenium(II) complexes [Ru(DIP) 2 (BIP)](PF 6) 2 (DIP = 4,7-diphenyl-1,10-phenanthrolie, BIP = 2-(1,1′-biphenyl-4-yl)-1 H -imidazo[4,5-f][1,10]phenanthroline, Ru1) and [Ru(DIP) 2 (CBIP)](PF 6) 2 (CBIP = 2-(4′-chloro-1,1′-biphenyl-4-yl)-1 H -imidazo[4,5-f][1,10]phenanthroline, Ru2) were synthesized. The cytotoxic activities in vitro of Ru1, Ru2 toward B16, A549, HepG2, SGC-7901, HeLa, BEL-7402, non-cancer LO2 were investigated using MTT method (3-(4,5-dimethylthiazole)-2,5-diphenltetraazolium bromide). Unexpectedly, Ru1, Ru2 can't prevent these cancer cells proliferation. To improve the anti-cancer effect, we used liposomes to entrap the complexes Ru1, Ru2 to form Ru1lipo, Ru2lipo. As expectation, Ru1lipo and Ru2lipo exhibit high anti-cancer efficacy, especially, Ru1lipo (IC 50 3.4 ± 0.1 μM), Ru2lipo (IC 50 3.5 ± 0.1 μM) display strong ability to block the cell proliferation in SGC-7901. The cell colony, wound healing, and cell cycle distribution show that the complexes can validly inhibit the cell growth at G2/M phase. Apoptotic studied with Annex V/PI doubling method showed that Ru1lipo and Ru2lipo can effectively induce apoptosis. Reactive oxygen species (ROS), malondialdehyde, glutathione and GPX4 demonstrate that Ru1lipo and Ru2lipo improve ROS and malondialdehyde levels, inhibit generation of glutathione, and finally result in a ferroptosis. Ru1lipo and Ru2lipo interact on the lysosomes and mitochondria and damage mitochondrial dysfunction. Additionally, Ru1lipo and Ru2lipo increase intracellular Ca2+ concentration and induce autophagy. The RNA-sequence and molecular docking were performed, the expression of Bcl-2 family was investigated by Western blot analysis. Antitumor in vivo experiments confirm that 1.23 mg/kg, 2.46 mg/kg of Ru1lipo possesses a high inhibitory rate of 53.53% and 72.90% to prevent tumor growth, hematoxylin-eosin (H&E) results show that Ru1lipo doesn't cause chronic organ damage and strongly promotes the necrosis of solid tumor. Taken together, we conclude that Ru1lipo and Ru2lipo cause cell death through the following pathways: autophagy, ferroptosis, ROS-regulated mitochondrial dysfunction, and blocking the PI3K/AKT/mTOR. Two new Ru(II) polypyridyl complexes [Ru(dip) 2 (BIP)](PF 6) 2 (dip = 4,7-diphenyl-1,10-phenanthrolie, BIP = 2-(1,1′-biphenyl-4-yl)-1 H -imidazo[4,5-f] [1,10]phenanthroline, Ru1) and [Ru(dip) 2 (CBIP)](PF 6) 2 (CBIP = 2-(4′-chloro-1,1′-biphenyl-4-yl)-1 H -imidazo[4,5-f] [1,10]phenanthroline, Ru2) and complexes-loaded liposomes Ru1lipo and Ru2lipo were synthesized and characterized. The cytotoxicity of the complexes Ru1, Ru2, Ru1lipo and Ru2lipo against B16, BEL-7402, A549, HepG2, SGC-7901 cancer cells and non-cancer cell LO2 was evaluated using 3-(4,5-dimethylthiazole-2-yl)-2,5-biphenyl tetrazolium bromide (MTT) method. The high inhibitory rate in vivo of Ru1lipo inhibiting SGC-7901 tumor growth reaches 72.90%. [Display omitted] • Two new Ru(II) polypyridyl complexes were synthesized and characterized. • The cytotoxicity in vitro and in vivo of the complexes and liposomes was investigated. • Apoptosis, reactive oxygen species and cell cycle arrest were performed. • RNA-sequence assay was investigated. • The antitumor activity in vivo was investigated. [ABSTRACT FROM AUTHOR]

• The self-crystallization and self-repair characters of perovskite thin films were revealed. • The association mechanism was systematically studied between the self-crystallization and the improving of the PSCs photovoltaic performances. • The self-crystallization of perovskite films could optimize grain orientation, reduce defects density and Urbach energy, and increase carrier fluorescence lifetime and transportation. When the perovskite solar cells (PSCs) had been stored in glove box for 2 days, the improvement of devices performance was observed. The mechanism of this phenomenon was systematically studied by using the in-situ XRD and in-situ absorption spectrum in this paper. It was revealed that the self-crystallization and self-repair characters of (FAPbI 3) 1- x (MAPbBr 3) x films were the keys to improve devices performance at room temperature. Then, we systematically studied the effects of self-crystallization based on grain orientation, crystalline quality, optical absorption properties, Urbach energy, defects density, carrier fluorescence lifetime etc. After self-crystallization, the defects density of (FAPbI 3) 1- x (MAPbBr 3) x thin films was decreased by about 22.9%, the carrier fluorescence lifetime was extended by about 1.68 times, and the Urbach energy was also reduced. These results indicated that the self-crystallization and self-repair of perovskite films could suppress the defect-assisted recombination, reduce the V OC loss, and enhance carrier transportation properties, which contributed to the improvement of the PSCs photovoltaic performance. [Display omitted] The self-crystallization and self-repair characters of (FAPbI 3) 1- x (MAPbBr 3) x films was revealed by using the in-situ XRD and in-situ absorption spectrum in this paper. The self-crystallization and self-repair of perovskite films could suppress the defect-assisted recombination, reduce the V OC loss, and enhance carrier transportation properties. which contributed to the improvement of the PSCs photovoltaic performance. [ABSTRACT FROM AUTHOR]

In this study, two new iridium(III) polypyridyl complexes [Ir(bzq) 2 (DIPH)](PF 6) (bzq = deprotonated benzo[ h ]quinoline, DIPH = 4-(2,5-dibromo-4-(1 H -imidazo[4,5-f][1,10]phenanthrolim-2-yl)-4-hydroxybutan-2-one) (Ir1) and [Ir(piq) 2 (DIPH)](PF 6) (piq = deprotonated 1-phenylisoquinoline) (Ir2) were synthesized and characterized by elemental analysis, HRMS, 1H and 13C NMR. The cytotoxic activity of Ir1 , Ir2 , Ir1lipo and Ir2lipo against cancer cells SGC-7901, HepG2, A549, HeLa, B16 and normal NIH3T3 cells in vitro was evaluated using 3-(4,5-dimethylthiazole-2-yl)-2,5-biphenyl tetrazolium bromide (MTT) method. Ir1 and Ir2 showed no cytotoxic activity, but their liposome-entrapped Ir1 (Ir1lipo) and Ir2 (Ir2lipo) showed significant cellular activity, especially sensitive to SGC-7901 with IC 50 values of 4.7 ± 0.2 and 12.4 ± 0.5 μM, respectively. The cellular uptake, endoplasmic reticulum (ER) localization, autophagy, tubulin polymerization, glutathione (GSH), malondialdehyde (MDA) and release of cytochrome c were investigated to explore the mechanisms of apoptosis. The calreticulin (CRT), heat shock protein 70 (HSP70), high mobility group box 1 (HMGB1) were also explored. Western blotting showed that Ir1lipo and Ir2lipo inhibited PI3K (phosphoinositide-3 kinase), AKT (protein kinase B), p-AKT and activated Bcl-2 (B-cell lymphoma-2) protein and apoptosis-regulated factor caspase 3 (cysteinyl aspartate specific proteinase-3) and cleaving PARP (poly ADP-ribose polymerase). The results demonstrated that Ir1lipo and Ir2lipo induce cell apoptosis through targeting the endoplasmic reticulum (ER), cause oxidative stress damage, inhibiting PI3K/AKT signaling pathway, immunogenic cell death (ICD) and inhibit the cell growth at G2/M phase. Two new iridium(III) complexes were synthesized and characterized. The anticancer activity of the liposome-entrapped complexes against SGC-7901 cells were investigated, the liposome-entrapped complexes exhibit high anticancer activity toward SGC-7901 cells. [Display omitted] • Two iridium(III) complexes and liposomes was synthesized and characterized. • The cytotoxicity of the complexes and their liposomes was investigated. • Apoptosis, reactive oxygen species and cell cycle arrest were carried out. • The immunogenic cell death and molecular docking were performed. • The expression of B-cell lymphoma-2 family proteins was examined. [ABSTRACT FROM AUTHOR]

Silver nanowire (AgNW) transparent conductive films (TCFs) are expected to replace ITO films due to their high transmissivity, conductivity, and flexibility. However, there are high junction resistance and poor inoxidizability of AgNW-TCFs. Instead of sputtering a metal oxide film on the surface of AgNW-TCFs, we apply metal oxide nanoparticles (MONPs) via magnetron sputtering to modify the AgNWs network. The goal is to reduce junction resistance of wire-wire junctions while wrapping AgNWs in a manner that improves the stability of AgNWs-TCFs. SnO 2 , ZnO, Al 2 O 3 , and TiO 2 are used as modification materials, and the AgNWs@MONPs-TCF with like-core–shell structures are obtained via magnetron sputtering. The resistance of AgNWs@MONPs-TCFs is lower by about 50% than that of the reference (AgNW-TCFs). The resistance nonuniformities of the AgNWs, AgNWs@SnO 2 , AgNWs@ZnO, AgNWs@Al 2 O 3 , and AgNWs@TiO 2 TCFs are 12%–13.2%, 6.9%, 9.8%, 10.3%, and 11.1%, respectively. After 28 days, their resistance has been increased 328.2%, 18.4%, 24.3%, 24.1%, and 35.7%, respectively. At 155 °C, their non-uniformity of temperature is 35.6%, 17.7%, 16.9%, 24.8%, and 23.2%, respectively. Comparing with the reference, their failure voltage and their electric-heating efficiency have been significantly improved by MONPs modification. Using the AgNWs@SnO 2 -TCFs as a transparent heating film in electric ceramic teacups, a good electric heating effect and stable performance have presented. [ABSTRACT FROM AUTHOR]

Organometal lead halides perovskites are promising solar cells material due to their outstanding properties such as tuneable bandgap, impressive tolerance to defects, long exciton diffusion length, high carrier mobility and absorption coefficient. Up to now, the organometal lead halides based solar cells (PSCs) have demonstrated impressive power conversion efficiency reaching 25.2% (not stabilised). However, their operating life-times are limited due to degradation of the organic components under some environmental conditions. Therefore, researchers have focused their interest on the all inorganic perovskite; especially on the caesium lead triiodide perovskite (CsPbI 3) which exhibits a better compositional and chemical stability. Nevertheless, the phase instability of the black phase of this material constitutes its main limitation for its use in the solar cell devices production. This review aims to present the most impactful research giving insights on the factors that may cause the instability of all-inorganic lead halide perovskite materials, as well as the instability of the whole device. In addition to deposition methods, the composition, structure and optical properties of inorganic perovskite materials have also been presented. Furthermore, this review highlights the different strategies used in order to improve the phase stability of caesium lead halide perovskite material through either engineering on the material structure or the fabrication method. Image 1 • The most relevant studies on the stability of all-inorganic PSCs materials and preparation methods are reviewed. • The effects of different engineering/modifications methods on the phase stability of CsPbI 3 are reviewed. • The influence of the different layers on the device efficiency and stability are pointed out. [ABSTRACT FROM AUTHOR]

Iridium(III) complexes are largely studied as anti-cancer complexes due to their excellent anti-cancer activity. In this article, two new iridium(III) complexes [Ir(piq) 2 (THPIP)]PF 6 (THPIP = 2,4-di-tert-butyl-6-(1 H -imidazo[4,5-f][1,10]phenanthrolin-2-yl)phenol, piq = deprotonated 1-phenylisoquinoline) (Ir1) and [Ir(bzq) 2 (THPIP)]PF 6 (bzq = deprotonated benzo[ h ]quinolone) (Ir2) were synthesized. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays showed that complex Ir1 exhibits moderate activity (IC 50 = 29.9 ± 4.6 μM) and Ir2 shows high cytotoxicity (IC 50 = 9.8 ± 1.8 μM) against BEL-7402 cells. Further studies on the mechanism showed that Ir1 and Ir2 induced apoptosis by changing the mitochondrial membrane potential, Ca2+ release, ROS accumulation, and cell cycle arrest at the S phase. The complexes can effectively inhibit cell colony formation and migration. The expression of B-cell lymphoma-2 (Bcl-2) family proteins, PI3K (phosphatidylinositol 3-kinase), AKT (protein kinase B), mTOR (mammalian target of rapamycin), and p-mTOR was studied by immunoblotting. Complexes Ir1 and Ir2 downregulated the expression of anti-apoptotic protein Bcl-2 and increased the expression of autophagy-related proteins of Beclin-1 and LC3-II. Further experiments showed that the complexes inhibited the production of glutathione (GSH) and increased the amounts of malondialdehyde (MDA). Fluorescence of HMGB1 was significantly increased. We also investigated the effect of the complexes on the expression of genes using RNA-sequence analysis, we further calculated the lowest binding energies between the complexes and proteins using molecular docking. Taken together, the above results indicated that complexes Ir1 and Ir2 induce apoptosis in BEL-7402 cells through a ROS-mediated mitochondrial dysfunction and inhibition of the PI3K/AKT/mTOR signaling pathway. Two new iridium(III) complexes were synthesized and characterized. The anticancer activity of the complexes against BEL-7402 cells were studied, the complexes display high anticancer activity toward BEL-7402 cells. [Display omitted] • Two new iridium(III) complex was synthesized and characterized. • The cytotoxicity in vitro of the complexes was studied. • Apoptosis, reactive oxygen species and cell cycle arrest were carried out. • The RNA-sequence was assayed. • The expression of B-cell lymphoma-2 family proteins was examined. [ABSTRACT FROM AUTHOR]

In this article, four new Ru(II) complexes [Ru(dmbpy) 2 (TFBIP)](PF 6) 2 (dmbpy = 4,4′-dimethyl-2,2′-bipyridine, TFPIP = 2-(4′-trifluoromethyl)-[1,1′-biphenyl]-4-yl)-1 H -imidazo[4,5-f][1,10]phenanthroline) (Ru1), [Ru(bpy) 2 (TFBIP)](PF 6) 2 (bpy = 2,2′-bipyridine) (Ru2), [Ru(phen) 2 (TFBIP)](PF 6) 2 (phen = 1,10-phenanthroline) (Ru3) and [Ru(dmp) 2 (TFBIP)](PF 6) 2 (dmp = 2,9-dimethyl-1,10-phenanthroline) (Ru4) were synthesized and characterized by elemental analysis, HRMS, IR, 1H NMR, 13C NMR and 19F NMR. The in vitro anticancer effect of the complexes on HepG2, A549, B16, HeLa, BEL-7402 and non-cancer LO2 cells was screened using 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) method. The results illustrate that the complexes display moderate anticancer activity. Apoptotic assay with Annexin V/PI double staining method indicated that complexes induce apoptosis in HepG2 cells. Also, the complexes interfere with the mitochondrial functions, accompanied by the production of intracellular ROS as well as a reduction of mitochondrial membrane potential. The results obtained from the western blot demonstrated that the complexes upregulate pro-apoptotic Bax and downregulate anti-apoptotic Bcl-2, which further activates caspase 3 and promotes the cleavage of PARP. RNA-sequence showed that the complexes upregulate the expression of 40 genes and downregulate 66 genes. Antitumour in vivo demonstrated that Ru1 inhibits the tumor growth with a high inhibitory rate of 51.19%. Taken together, these results revealed that complexes Ru1 , Ru2 , Ru3 and Ru4 induce cell death in HepG2 cells via autophagy and a ROS-mediated mitochondrial apoptotic pathway. Four new Ru(II) complexes were synthesized and characterized. The anticancer activity of the complexes against HepG2 cells were investigated, the complexes display high antitumour efficacy in vivo. [Display omitted] • Four new Ru(II) complex were synthesized and characterized. • The cytotoxicity in vitro and in vivo of the complexes was investigated. • Apoptosis, reactive oxygen species and cell cycle arrest were detected. • The RNA-sequence was determined. • The expression of B-cell lymphoma-2 family proteins was examined. [ABSTRACT FROM AUTHOR]