Research on materials with pure organic room temperature phosphorescence (RTP) and their application as organic single-molecule white light emitters is a hot area and relies on the design of highly efficient pure organic RTP luminogens. Herein, a facile strategy of heavy-atom-participated anion–π+ interactions is proposed to construct RTP-active organic salt compounds (1,2,3,4-tetraphenyloxazoliums with different counterions). Those compounds with heavy-atom counterions (bromide and iodide ions) exhibit outstanding RTP due to the external heavy atom effect via anion–π+ interactions, evidently supported by the single-crystal X-ray diffraction analysis and theoretical calculation. Their single-molecule white light emission is realized by tuning the degree of crystallization. Such white light emission also performs well in polymer matrices and their use in 3D printing is demonstrated by white light lampshades.

Recent years have witnessed the significant role of anion-π interactions in many areas, which potentially brings the opportunity for the development of aggregation-induced emission (AIE) systems. Here, a new strategy that utilized anion-π interactions to block detrimental π-π stacking was first proposed to develop inherent-charged AIE systems. Two AIE-active luminogens, namely, 1,2,3,4-tetraphenyloxazolium (TPO-P) and 2,3,5-triphenyloxazolium (TriPO-PN), were successfully synthesized. Comprehensive techniques such as single-crystal analysis, theoretical calculation, and conductivity measurement were used to illustrate the effects of anion-π interactions on the AIE feature. Their analogues tetraphenylfuran (TPF) and 2,4,5-triphenyloxazole (TriPO-C) without anion-π interactions suffered from the aggregation-caused emission quenching in the aggregate state, demonstrating the important role of anion-π interactions in suppressing π-π stacking. TriPO-PN was biocompatible and could specifically target lysosome in fluorescence turn-on and wash-free manners. This suggested that it was a promising contrast agent for bioimaging.

Fibroblast growth factor 23 (FGF23) has been reported to induce left ventricular hypertrophy, but it remains unclear whether FGF23 plays a role in cardiac fibrosis. This study is attempted to investigate the role of FGF23 in post-infarct myocardial fibrosis in mice. We noted that myocardial and plasma FGF23 and FGF receptor 4 were increased in mice with heart failure as well as in cultured adult mouse cardiac fibroblasts (AMCFs) exposed to angiotensin II, phenylephrine, soluble fractalkine. Recombinant FGF23 protein increased active β-catenin , procollagen I and procollagen III expression in cultured AMCFs. Furthermore, intra-myocardial injection of adeno-associated virus-FGF23 in mice significantly increased left ventricular end-diastolic pressure and myocardial fibrosis, and markedly upregulated active β-catenin, transforming growth factor β (TGF-β), procollagen I and procollagen III in both myocardial infarction (MI) and ischemia/reperfusion (IR) mice, while β-catenin inhibitor or silencing of β-catenin antagonized the FGF23-promoted myocardial fibrosis in vitro and in vivo. These findings indicate that FGF23 promotes myocardial fibrosis and exacerbates diastolic dysfunction induced by MI or IR, which is associated with the upregulation of active β-catenin and TGF-β.

Ischemic stroke, producing a high mortality and morbidity rate, is a common clinical disease. Enhancing the prevention and control of ischemic stroke is particularly important. Baicalin and its aglycon baicalein are flavonoids extracted from Scutellaria baicalensis, an important traditional Chinese herb. In recent years, a growing body of evidences has shown that baicalin and baicalein could be effective in the treatment of cerebral ischemia. Pharmacokinetic studies have shown that baicalin could penetrate the blood-brain barrier and distribute in cerebral nuclei. Through a variety of in vitro and in vivo models of ischemic neuronal injury, numerous studies have demonstrated that baicalin and baicalein have salutary effect for neuroprotection. Especially, the studies on the pharmacological mechanism showed that baicalin and baicalein have several pharmacological activities, which include antioxidant, anti-apoptotic, anti-inflammatory and anti-excitotoxicity effects, protection of the mitochondria, promoting neuronal protective factors expression and adult neurogenesis effects and many more. This review focuses on the neuroprotective effects of baicalin and baicalein in ischemia or stroke-induced neuronal cell death. We aimed at collecting all important information regarding the neuroprotective effect and its pharmacological mechanism of baicalin and baicalein in various in vivo and in vitro experimental models of ischemic neuronal injury.

A series of organic host–guest materials with multifunctional luminescence were constructed. Four isoquinoline derivatives were used as the guests, and benzophenone was used as the host. The doped system exhibited excellent dual emission with cyan fluorescence and orange-yellow room-temperature phosphorescence, and the dual emission could be combined into almost pure white-light emission. Importantly, the relative intensity of the fluorescence–phosphorescence could be adjusted by changing the excitation wavelength, with the phosphorescence intensity being significantly higher than the fluorescence intensity under shorter excitation wavelengths and vice versa under longer excitation wavelengths. Therefore, three-color emission switching among cyan, white, and orange could be achieved by simply adjusting the excitation wavelength. The results of experimental and theoretical calculations indicated that the excitation-dependent emission colors were caused by different transfer paths for excitons under different excitation wavelengths. These materials with multifunctional luminescence could be used as writable inks for advanced anticounterfeiting.

Despite the great potential of heteroatom-containing polycyclic aromatic hydrocarbons in organic optoelectronics, there are very limited reports on heteroaromatics containing a B-N-B bond in the π-scaffold. Herein, stable 1,9-dibora-9a-azaphenalenyl (DBAP) derivatives, named BNB-embedded phenalenyls, are presented. The DBAP skeleton contains a three-center two-π-electron B-N-B moiety with 12 π-electrons and can be regarded as the isoelectronic structure of the phenalenyl cation. Chemical reduction of the phenyl derivative of DBAP by potassium generated the dianion containing 14 delocalized π-electrons, which can be regarded as the isoelectronic structure of the phenalenyl anion. The dianion is sandwiched and stabilized by two bulky [K([18]crown-6)] counterions according to its X-ray structure. However, its monoanion (an isoelectronic structure of the henalenyl radical) generated by mixing equal moles of neutral compound and dianion gave an unusual B-N-B-embedded benzo[cd]fluoranthene dianion, which again was confirmed by X-ray crystallographic analysis. The new dianion containing 20 π-electrons is highly aromatic and is further stabilized by [K([18]crown-6)] counterions. An aromaticity driven rearrangement mechanism was proposed for this unusual transformation. Based on X-ray structures and theoretical calculations, the B-N-B moiety in the neutral and anionic DBAP participates in the π-electron delocalization along the whole DBAP skeleton like their phenalenyl cation/radical/anion counterparts, but with more localized character. Therefore, our studies report the first synthesis and characterization of a B-N-B-embedded phenalenyl and its anionic species, which show unique electronic structure and unusual reactivity different from that of their all-carbon phenalenyl analogues.

An efficient Pd-catalyzed copper and amine free coupling reaction of acetylene and aryl bromides was achieved with calcium carbide as an acetylene source, using inorganic base and easily prepared, air-stable aminophosphine ligand in common organic solvents, providing symmetric diaryl ethynes in one-pot with yields ranged from moderate to excellent.

AimsTo resolve the controversy as to whether periostin plays a role in myocardial regeneration after myocardial infarction (MI), we created a neonatal mouse model of MI to investigate the influence of periostin ablation on myocardial regeneration and clarify the underlying mechanisms.Methods and resultsNeonatal periostin-knockout mice and their wildtype littermates were subjected to MI or sham surgery. In the wildtype mice after MI, fibrosis was detectable at 3 days and fibrotic tissue was completely replaced by regenerated myocardium at 21 days. In contrast, in the knockout mice, significant fibrosis in the infarcted area was present at even 3 weeks after MI. Levels of phosphorylated-histone 3 and aurora B in the myocardium, detected by immunofluorescence and western blotting, were significantly lower in knockout than in wildtype mice at 7 days after MI. Similarly, angiogenesis was decreased in the knockout mice after MI. Expression of both the endothelial marker CD-31 and α-smooth muscle actin was markedly lower in the knockout than in wildtype mice at 7 days after MI. The knockout MI group had elevated levels of glycogen synthase kinase (GSK) 3β and decreased phosphatidylinositol 3-kinase (PI3K), phosphorylated serine/threonine protein kinase B (p-Akt), and cyclin D1, compared with the wildtype MI group. Similar effects were observed in experiments using cultured cardiomyocytes from neonatal wildtype or periostin knockout mice. Administration of SB216763, a GSK3β inhibitor, to knockout neonatal mice decreased myocardial fibrosis and increased angiogenesis in the infarcted area after MI.ConclusionAblation of periostin suppresses post-infarction myocardial regeneration by inhibiting the PI3K/GSK3β/cyclin D1 signalling pathway, indicating that periostin is essential for myocardial regeneration.