Macrocycle Self-Assembly Hydrogel for High-Efficient Oil-Water Separation.

Supramolecular hydrogels involved macrocycles have been explored widely in recent years, but it remains challenging to develop hydrogel based on solitary macrocycle with super gelation capability. Here, the construction of lantern[33 ]arene-based hydrogel with low critical gelation concentration (0.05 wt%), which can be used for efficient oil-water separation, is reported. The lantern[33 ]arenes self-assemble into hydrogen-bonded organic nanoribbons, which intertwine into entangled fibers to form hydrogel. This hydrogel which exhibits reversible pH-responsiveness characteristics can be coated on stainless-steel mesh by in situ sol-gel transformation. The resultant mesh exhibits excellent oil-water separation efficiency (>99%) and flux (>6 × 104 L m-2 h-1 ). This lantern[33 ]arene-based hydrogel not only sheds additional light on the gelation mechanisms for supramolecular hydrogels, but also extends the application of macrocycle-based hydrogels as functional interfacial materials.

Overcoming chemoresistance in non-angiogenic colorectal cancer by metformin via inhibiting endothelial apoptosis and vascular immaturity.

The development of chemoresistance which results in a poor prognosis often renders current treatments for colorectal cancer (CRC). In this study, we identified reduced microvessel density (MVD) and vascular immaturity resulting from endothelial apoptosis as therapeutic targets for overcoming chemoresistance. We focused on the effect of metformin on MVD, vascular maturity, and endothelial apoptosis of CRCs with a non-angiogenic phenotype, and further investigated its effect in overcoming chemoresistance. In situ transplanted cancer models were established to compare MVD, endothelial apoptosis and vascular maturity, and function in tumors from metformin- and vehicle-treated mice. An in vitro co-culture system was used to observe the effects of metformin on tumor cell-induced endothelial apoptosis. Transcriptome sequencing was performed for genetic screening. Non-angiogenic CRC developed independently of angiogenesis and was characterized by vascular leakage, immaturity, reduced MVD, and non-hypoxia. This phenomenon had also been observed in human CRC. Furthermore, non-angiogenic CRCs showed a worse response to chemotherapeutic drugs in vivo than in vitro. By suppressing endothelial apoptosis, metformin sensitized non-angiogenic CRCs to chemo-drugs via elevation of MVD and improvement of vascular maturity. Further results showed that endothelial apoptosis was induced by tumor cells via activation of caspase signaling, which was abrogated by metformin administration. These findings provide pre-clinical evidence for the involvement of endothelial apoptosis and subsequent vascular immaturity in the chemoresistance of non-angiogenic CRC. By suppressing endothelial apoptosis, metformin restores vascular maturity and function and sensitizes CRC to chemotherapeutic drugs via a vascular mechanism.

Metformin enhances T lymphocyte anti-tumor immunity by increasing the infiltration via vessel normalization.

Abnormal tumor vasculature blocks the extravasation of T lymphocytes into the tumor, thereby suppressing anti-tumor immunity. Recently, metformin has been shown to affect tumor vasculature and enhance T lymphocyte anti-tumor immunity. However, whether or how metformin affects T lymphocyte anti-tumor immunity via a vascular mechanism remains poorly understood. Herein, we show that a large number of CD8+ lymphocytes gathered in the peri-tumoral region, while very few infiltrated the tumor. Metformin administration increased the expression of anti-tumor immunity-associated genes and the number of tumor-infiltrating CD8+ lymphocytes. Injection of CD8 but not CD4 neutralization antibody into tumor-bearing mice significantly abrogated the anti-tumor effect of metformin. Critically, CD8+ lymphocytes were found to pass through the wall of perfused vessel. Further results of immunofluorescent staining showed that metformin greatly elevated tumor perfusion, which was accompanied by increased vascular maturity in the intratumoral region (ITR) but not peritumoral region (PTR). These findings provide evidence for the vascular mechanism involved in metformin-induced enhancement of T lymphocyte anti-tumor immunity. By remodeling the abnormal tumor vasculature, also called vessel normalization metformin increases vascular maturity and tumor perfusion, thus allowing more CD8+ lymphocytes to infiltrate the tumor.

Icariside II Attenuates Vascular Remodeling Via Wnt7b/CCND1 Axis.

ABSTRACT: Angioplasty often fails due to the abnormal proliferation of vascular smooth muscle cells (VSMCs). Success rates of angioplasty may increase following the administration of an agent that effectively ameliorates aberrant vascular remodeling. Icariside II (ICS-II) is a natural flavonol glycoside extract from the Chinese herbal medicine Epimedii that possesses several medicinal qualities that are beneficial in humans. Nevertheless, the role of ICS-II in addressing aberrant vascular remodeling have yet to be clarified. The current investigation studies the molecular effects of ICS-Ⅱ on balloon-inflicted neointimal hyperplasia in rats in vivo and on platelet-derived growth factor-induced vascular proliferation in primary rat aortic smooth muscle cells (VSMCs) in vitro. ICS-II was found to be as effective as rapamycin, the positive control used in this study. ICS-II inhibited neointimal formation in injured rat carotid arteries and notably reduced the expression of Wnt7b. ICS-Ⅱ significantly counteracted platelet-derived growth factor-induced VSMCs proliferation. Cell cycle analysis showed that ICS-II triggered cell cycle arrest during the G1/S transition. Western blot analysis further indicated that this cell cycle arrest was likely through Wnt7b suppression that led to CCND1 inhibition. In conclusion, our findings demonstrate that ICS-II possesses significant antiproliferative qualities that counteracts aberrant vascular neointimal hyperplasia. This phenomenon most likely occurs due to the suppression of the Wnt7b/CCND1 axis.

Steric hindrance effect on the excited-state proton transfer process: TDDFT study on the fluorescent sensing mechanism of a fluoride sensor.

An understanding of the excited-state process and the sensing mechanism for specific anions can be helpful for the design and synthesis of fluorescent sensors in analytical chemistry and biotechnology. Here, we theoretically investigated the fluorescent response mechanism of a reported acylhydrazone-based fluorescent sensor (Soft Matter, 2019, 15, 6690) for fluoride recognition using the time-dependent density functional theory approach. At the M06/TZVP/SCM level, the vertical excitation energies, which were calculated based on the ground state and first singlet-state geometries of the sensor molecule, agreed well with the experimental ultraviolet-visible and fluorescence spectra. Therefore, the time-dependent density functional theory method was considered reasonable and effective. According to the frontier orbital analysis and an excited-state potential energy scan, we proposed an excited-state proton transfer mechanism for the sensor-fluorine complex, where the steric hindrance leads to a high potential barrier. The excited-state proton transfer process facilitates sensor molecule deprotonation, alleviates its steric hindrance effect and expands its conjugated system. As a result, the fluorescence emission band of the sensor molecule was red-shifted significantly with the addition of fluoride anion. Based on this fluorescence difference, the sensor could be used for fluoride anion identification. This work provides a strategy to study sensor-analyte interactions in the excited state and offers an approach to tune the fluorescence emission wavelength of sensor molecules in anionic environments.

Metformin inhibits metastatic breast cancer progression and improves chemosensitivity by inducing vessel normalization via PDGF-B downregulation.

BACKGROUND: Vascular maturity and functionality are closely associated with tumor progression and chemosensitivity. The antidiabetic agent metformin has shown its ability to inhibit tumor angiogenesis in metastatic breast cancer models. However, it remains unclear if or how metformin remodels the abnormal vasculature of metastatic breast cancer, while inhibiting angiogenesis. METHODS: Metastatic breast cancer models were constructed to compare microvessel density (MVD), vascular maturity and function, lung metastasis and chemosensitivity in metformin-treated or untreated mice. Protein array assay and transcriptome sequencing were performed for genetic screening. Lentiviral shRNA-PDGF-B transfection was used for observing the contribution of PDGF-B knockdown to metformin's vascular effects. RESULTS: Metastatic breast cancers were characterized by an excessively angiogenic, immature and morphologically abnormal vasculature. Compared to control, metformin significantly reduced MVD, leakage and hypoxia, and increased vascular mural cells coverage and perfusion, namely, "vessel normalization". Metformin at human blood concentrations had no direct effect on the migration and proliferation of cancer cells. Based on that, reduced lung metastasis of the primary tumor and improved chemosensitization by metformin were assumed to be mediated via metformin's vascular effects. Further results of genetic screening and in vivo experiments showed that the downregulation of platelet-derived growth factor B (PDGF-B) greatly contributed to the metformin-induced vessel normalization. CONCLUSIONS: These findings provide pre-clinical evidences for the vascular mechanism of metformin-induced metastasis inhibition and the chemosensitization of metastatic breast cancers.

TDDFT study on aluminum and fluoride dual-sensing mechanism of a Schiff-Base sensor.

The aluminum and fluoride dual-sensing mechanism of a previously reported sensor with a Schiff-base moiety (Spectrochim. Acta A, 2017, 183, 267-274) has been investigated by density functional theory (DFT) and time-dependent DFT (TDDFT) methods. The present calculations reproduce the photoproperties of the sensor as well as its aluminum and fluoride complexes, which illustrates that DFT and TDDFT constitute a reliable tool for uncovering detailed fluorescence-based sensing mechanisms in diverse electronic states. Theoretical results indicate that there are two OH⋯N hydrogen bonds in the sensor and two OH⋯F hydrogen bonds in its F¯ complex. Different degrees of coplanarity caused by these hydrogen bonds are responsible for their distinct absorption wavelengths. However, excited-state geometry optimization and a scan of the potential-energy surface show that there is twisted intramolecular charge transfer about the CN bond in the sensor molecule and an excited-state proton-transfer process from the fluoride anion to the neighboring N atom in the fluoride-sensor complex, whereby the fluorescence is quenched. A chelation-enhanced fluorescence effect associated with the aluminum-sensor complex shows a different excited-state process. The local excitation and emission occur exclusively within the planar fluorophore, and negligible structural change upon excitation of the aluminum-sensor complex leads to its strong fluorescence. Therefore, it is theoretically explained why the sensor may be successfully used to analyze the fluoride anion by absorption spectroscopy and the aluminum cation by emission spectroscopy.

Metformin's antitumour and anti-angiogenic activities are mediated by skewing macrophage polarization.

Beneficial effects of metformin on cancer risk and mortality have been proved by epidemiological and clinical studies, thus attracting research interest in elucidating the underlying mechanisms. Recently, tumour-associated macrophages (TAMs) appeared to be implicated in metformin-induced antitumour activities. However, how metformin inhibits TAMs-induced tumour progression remains ill-defined. Here, we report that metformin-induced antitumour and anti-angiogenic activities were not or only partially contributed by its direct inhibition of functions of tumour and endothelial cells. By skewing TAM polarization from M2- to M1-like phenotype, metformin inhibited both tumour growth and angiogenesis. Depletion of TAMs by clodronate liposomes eliminated M2-TAMs-induced angiogenic promotion, while also abrogating M1-TAMs-mediated anti-angiogenesis, thus promoting angiogenesis in tumours from metformin treatment mice. Further in vitro experiments using TAMs-conditioned medium and a coculture system were performed, which demonstrated an inhibitory effect of metformin on endothelial sprouting and tumour cell proliferation promoted by M2-polarized RAW264.7 macrophages. Based on these results, metformin-induced inhibition of tumour growth and angiogenesis is greatly contributed by skewing of TAMs polarization in microenvironment, thus offering therapeutic opportunities for metformin in cancer treatment.

A Comparison of Concomitant Tributary Laser Ablation and Foam Sclerotherapy in Patients Undergoing Truncal Endovenous Laser Ablation for Lower Limb Varicose Veins.

PURPOSE: To compare outcomes of patients who received simultaneous tributary endovenous laser ablation (EVLA) or foam sclerotherapy (FS) with EVLA of the great saphenous vein (GSV) trunk. METHODS AND MATERIALS: This study recruited 418 patients (542 legs) with diagnosed varicose veins. Patients in the EVLA/FS group (255 patients, 327 legs) received concomitant FS for the tributaries with truncal lasering. For the EVLA-alone group (163 patients, 215 legs), tributaries (8W) were ablated with EVLA in addition to the GSV trunk (14W). Complications, Aberdeen Varicose Vein Questionnaire (AVVQ), EuroQol Group 5-Dimension Self-Report Questionnaire (EQ-5D), numerical rating scale (NRS) scores, and condition of residual varicosities were assessed at 3 days, 4 weeks, and 6 months after procedure. All residual varicosities were identified and treated with a staged FS at 6 months. RESULTS: Except for ecchymosis, incidence of other complications was not significantly different between both groups at 6 months. Pain NRS scores of the EVLA/FS group were remarkably elevated at 4 weeks and then, at 6 months, declined to a level similar to the EVLA-alone group. The EVLA/FS group exhibited more significant improvement in both AVVQ and EQ-5D scales than the EVLA group at 6 months, while exhibiting poor improvement at 4 weeks. The EVLA/FS group had a significantly lower rate of residual varicosities than the EVLA group, thus reducing the need for the staged FS. CONCLUSIONS: These results confirm the feasibility and safety of simultaneous tributary EVLA and FS. In addition, they indicate better early quality-of-life improvement and a reduced reoperation rate of simultaneously combined truncal EVLA and tributary FS.

Activation of AMPK by simvastatin inhibited breast tumor angiogenesis via impeding HIF-1α-induced pro-angiogenic factor.

Substantial data from preclinical studies have revealed the biphasic effects of statins on cardiovascular angiogenesis. Although some have reported the anti-angiogenic potential of statins in malignant tumors, the underlying mechanism remains poorly understood. The aim of this study is to elucidate the mechanism by which simvastatin, a member of the statin family, inhibits tumor angiogenesis. Simvastatin significantly suppressed tumor cell-conditioned medium-induced angiogenic promotion in vitro, and resulted in dose-dependent anti-angiogenesis in vivo. Further genetic silencing of hypoxia-inducible factor-1α (HIF-1α) reduced vascular endothelial growth factor and fibroblast growth factor-2 expressions in 4T1 cells and correspondingly ameliorated HUVEC proliferation facilitated by tumor cell-conditioned medium. Additionally, simvastatin induced angiogenic inhibition through a mechanism of post-transcriptional downregulation of HIF-1α by increasing the phosphorylation level of AMP kinase. These results were further validated by the fact that 5-aminoimidazole-4-carboxamide ribonucleotide reduced HIF-1α protein levels and ameliorated the angiogenic ability of endothelial cells in vitro and in vivo. Critically, inhibition of AMPK phosphorylation by compound C almost completely abrogated simvastatin-induced anti-angiogenesis, which was accompanied by the reduction of protein levels of HIF-1α and its downstream pro-angiogenic factors. These findings reveal the mechanism by which simvastatin induces tumor anti-angiogenesis, and therefore identifies the target that explains the beneficial effects of statins on malignant tumors.

Suppression of hypoxia-induced excessive angiogenesis by metformin via elevating tumor blood perfusion.

The anti-diabetic metformin has been demonstrated to be effective in suppression of tumor progression via multiple mechanisms, in which angiogenic inhibition is involved. Hypoxia is a common feather of malignant tumor and promotes angiogenesis via induction of pro-angiogenic factors. However, the effect of metformin on tumor hypoxia and the association with angiogenic inhibition are still unclear. In the current study, we investigated the effects of metformin on both tumor blood perfusion and hypoxia-induced excessive angiogenesis. In the tumor region adjacent to necrosis, aberrantly excessive angiogenesis resulted from hypoperfusion-induced intense hypoxia and greatly contributed to the high average levels of both microvessel density and vascular branch density. Metformin administration increased the percentage of lectin-perfused vessels and reduced hypoxyprobe-positive area. This metformin-induced amelioration of hypoxia was accompanied by a significant reduction in expressions of both HIF-1α and angiogenesis-associated factors (AAFs). Consequently, inhibited excessive angiogenesis in hypoxic peri-necrotic region was observed in metformin-treated tumor. Further stable knockdown of HIF-1α abrogated hypoxia-induced AAFs in vitro and reduced both microvessel density and area of fitc-conjugated dextran that leaked outside the vascular lumen. Taken together, metformin ameliorated tumor hypoxia and restrained HIF-1α-induced expressions of AAFs through elevating tumor blood perfusion, thus suppressing the excessive tumor angiogenesis.

Molecular Characterization and Bioinformatics Analysis of a Prophenoloxidase-1 (PPO1) in Plutella xylostella.

Phenoloxidase (PO) is an important enzyme in insect life, which is involved in important physical functions, such as defensive encapsulation and melanization of foreign organisms and wound healing. In this study, we obtained a cDNA sequence of 2838 bp with 2049 open reading frames encoding 682 amino acids. The protein sequence deduced from the cDNA has high homology with the known PPO1 sequences of other lepidopterous insects. There were three conserved regions, including the two copper-binding sites characteristic of arthropod PPOs. The whole PxPPO1 DNA was also obtained with 7202 bp when the five fragments were stitched together and the overlapping sequences were deleted. The PxPPO1 DNA consists of 11 introns and 12 exons, and the homology is 99.9% when the exons are compared with the above cDNA. Moreover, the gene expression levels were also determined by semiquantitative polymerase chain reaction (PCR), Western blotting, and real-time quantitative PCR; the results indicated that PxPPO1 transcripts in the eggs and the fourth instar larvae were more abundant, followed by the second and the third instar larvae, prepupae, and pupa.

Bioreduction of U(VI) and stability of immobilized uranium under suboxic conditions.

In order to study the bioreduction of U(VI) and stability of immobilized uranium under suboxic conditions, microcosm were amended with ethanol, lactate and glucose, and incubated under suboxic conditions. During the incubation, total dissolved U in amended microcosms decreased from 0.95 mg/L to 0.03 mg/L. Pyrosequencing results showed that, the proportion of anaerobic microorganisms capable of reducing U(VI) under suboxic conditions was small compared with that under anoxic conditions; the proportion of aerobic and facultative anaerobic microorganisms capable of consuming the dissolved oxygen was large; and some of the facultative anaerobic microorganisms could reduce U(VI). These results indicated that different microbial communities were responsible for the bioreduction of U(VI) under suboxic and anoxic conditions. After the electron donors were exhausted, total dissolved U in the amended microcosms remained unchanged, while the U(VI)/U(IV) ratio in the solid phase of sediments increased obviously. This implied that the performance of bioreduction of the U(VI) can be maintained under suboxic condition.

TDDFT study on the sensing mechanism of a fluorescent sensor for fluoride anion: Inhibition of the ESPT process.

The fluoride-sensing mechanism of a reported salicylaldehyde-based sensor (J. Photochem. Photobiol. B 2014, 138, 75) has been investigated by the TDDFT method. The present theoretical study indicates that there is an excited-state proton transfer (ESPT) process from the phenolic O-H moiety to the neighbor N atom in the sensor. The added fluoride anion could capture the proton in the O-H moiety and the corresponding phenolic anion is formed, which could inhibit the ESPT process. The experimental UV/Vis and fluorescence spectra are well reproduced by the calculated vertical excitation energies. Frontier molecular orbital analysis indicates that the local excited state of phenolic anion is responsible for its enhanced fluorescence. Due to this reason, the sensor can be used to sense fluoride anion by monitoring the fluorescent change.

[Effect of two Pi deficiency syndrome models on the configuration and function of the skeletal muscle in mice].

OBJECTIVE: To observe the relation between Pi deficiency syndrome (PDS) and the configuration and functions of extensor digitorum longus (EDL)and soleus (SOL). METHODS: Totally 36 ICR mice were randomly divided into 3 groups according to weight matching principle, the control group, the exhausted group, and the rhubarb group, 12 in each group. Two PDS models were established by either purgation with rhubarb diarrhea (as Group A) or exhausted swimming plus sleep deprivation (as Group B).The cross sectional area (CSA) of type I and II fibers of extensor digitorum longus (EDL) and soleus (SOL), relative proportions of type I and II fibers were measured by m-ATPase histochemical method. The isotonic contraction and the maximum tetanus contraction of EDL and SOL were detected by PowerLab system. RESULTS: Compared with the control group, the body weight, body temperature, and the general health condition of PDS model rats obviously decreased; the spleen index and the thymus index were also lower; the maximal isotonic contraction and the maximum tetanus contraction obviously decreased; the cross section areas of EDL and SOL were reduced with loosely arranged cells. In EDL, the proportion of type I fibers was added and the proportion of type II fibers was lowered. In SOL, there was no change in the proportion of type I and type II fibers. CONCLUSIONS: EDL and SOL were obviously atrophied in the two PDS model mice. The type I fibers of SOL was more significantly atrophied in Group B.

Bioreduction of U(VI) in groundwater under anoxic conditions from a decommissioned in situ leaching uranium mine.

To determine whether the U(VI) in groundwater under anoxic conditions at a decommissioned in situ leaching (ISL) uranium mine could be bioreduced, groundwater samples containing suspended sediments were taken from the mine, experimental setup was fabricated, and the jar containing the groundwater in the setup was amended with ethanol and incubated under anoxic conditions. The variations of pH, chemical oxygen demand, nitrate, sulfate, U(VI), and dissolved oxygen (DO) concentrations were monitored during the incubation. U(VI) concentration dropped to 0.043 mg/L when the stimulated microorganisms were active, and it then increased to 0.835 mg/L within 10 days after the metabolism of the stimulated microorganisms was inhibited. The DO variation was observed in the amended jar during the incubation, and the metabolism of the stimulated microorganisms was found to affect the DO concentration. Firmicutes were found to be dominant in the sediments in the amended jar through the 16S rRNA pyrosequencing. The results indicate that it is possible to bioreduce U(VI) in the groundwater under anoxic conditions at the decommissioned ISL uranium mine by adding carbon source into it without removing the oxygen from it.

Phytoextraction of uranium from contaminated soil by Macleaya cordata before and after application of EDDS and CA.

This is the first report on using Macleaya cordata for phytoextraction of uranium from the uranium contaminated soil in the greenhouse. Macleaya M. cordata was found to increase uranium concentration in the soil solution by increasing the dissolved organic carbon (DOC). The amendment experiments with citric acid (CA) and [S,S]-ethylenediamine disuccinic acid (EDDS) at the rates of 1.0, 2.5, 5.0, and 10.0 mmol kg(-1) dry weight (DW) soil showed that EDDS was more efficient to increase uranium concentration in the shoot than CA when they were applied at the same rate. The applications of 5.0 mmol kg(-1) EDDS and 10.0 mmol kg(-1) CA were most appropriate for increasing uranium concentrations in the shoot of M. cordata. CA was more efficient to increase the solubility of uranium at the same application rates except for 2.5 mmol kg(-1) application rate. There was a linear correlation between the uranium concentration in the shoot and the average uranium concentration of one planted pot during 14 days in soil solution after the application of different rates of EDDS and CA, respectively (r(2) = 0.972, P < 0.01; r (2) = 0.948, P < 0.01), indicating that uranium uptake was dependent on the soluble uranium concentration. The Fe-U-DOC and Mn-U-DOC complexes were probably formed after the application of CA. Soil solution pH and Fe, Mn, Ca, and DOC concentrations in soil solution were found to be changed by the chelates.

Flubendiamide resistance and Bi-PASA detection of ryanodine receptor G4946E mutation in the diamondback moth (Plutella xylostella L.).

The extensive application of flubendiamide has led to increasingly prominent development of resistance in diamondback moth, Plutella xylostella. Here we report that the moderate and high level resistance to flubendiamide was identified in a laboratory-selected and two field-collected strains of P. xylostella. The resistance ratios were tested in the lab-selected resistant strains (R), and two field strains (BY and ZC). Compared with the S strain, the R strain showed extended larval development time, decreased pupation rate, emergencing rate, and male adult longevity. The realized heritability (h(2)=0.135) implies the high risk of flubendiamide resistance development in P. xylostella. A Bi-PASA (bi-directional PCR amplification of specific allele)-based method was successfully developed to detect the point mutation (G4946E) potentially causing flubendiamide resistance in diamondback moth, in which different fragments 866 bp + 340 bp, 866 bp+568 bp, and 866 bp+568 bp+340 bp were presented in SS, RR and RS stains, respectively. The predominant genotype was 83.33% SS homozygote in the S strain, 80.77% RR homozygote in ZC population, and 73.08% RS heterozygote in BY population, respectively. Current results showed the significant correlation between the frequencies of the allele carrying G4946E mutation (51.92%, 55.77% and 90.38% for R, BY and ZC, respectively) and the resistance ratios (40.72, 24.24 and 1779.24-folds for R, BY and ZC, respectively) in the three strains/populations. In addition, the relative PxRyR mRNA transcript level in the R strain was 2.938 ± 0.53 folds as compared with the S strain (1.0-fold).

Structural and spectral properties of a zinc(II) coordination polymer: a combined experimental and theoretical study.

A novel 1D zinc(II) coordination polymer [Zn(bbbm)Cl2]n (where bbbm=1,4-bis(N-benzimidazolyl)butane) was synthetized by ZnCl2 and bbbm ligand under hydrothermal conditions, and its structural and spectral properties were studied by both experimental and theoretical techniques. The center zinc(II) ion displays four-coordinated in a tetrahedral geometry by two chloride anions and two N atoms of distinct bbbm ligands. Adjacent chains are further connected into a 2D layer structure through π-π stacking interactions. Vibrational frequencies of [Zn(bbbm)Cl2]n have been calculated using DFT/B3LYP/TZVP method, and well reproduced IR data. Furthermore, the vertical excitation energies from time-dependent DFT calculation confirmed that the fluorescent peaks at 385nm and 450nm could respectively be assigned to the π→π(*) transition within the bbbm ligands and π→n transition from chloride anion to bbbm ligand.

The effect of the skeleton structure of flavanone and flavonoid on interaction with transferrin.

Transferrin has been exploited as a potential drug carrier for targeted drug delivery into cancer cells, which express high levels of transferrin receptors. In the present study, we identified specific structural features in flavonoids that were critical for binding to transferrin. Flavanone naringenin and flavonoid apigenin, two flavonoids with characteristic flavonoid core structures were selected for the study of the effects of C2-C3 single bond in the C-ring on transferrin binding. We determined the binding affinities by fluorescence quenching experiments and investigated the binding modes by CD spectra and molecular modeling. Our results demonstrated that naringenin bound transferrin with an affinity almost 100 times higher than that of apigenin attributed to its higher structural flexibility and lower acidity compared with apigenin. Our docking study showed that naringenin had stronger van der Waals interactions with transferrin, which was believed to contribute to its higher binding affinity. We also found that naringenin-binding induced greater increase in the α-helix content in transferrin than apigenin, suggesting that transferrin became more compact upon association with naringenin. Our study demonstrated that naringenin was a ligand for transferrin with good affinity. The results reported herein can facilitate the design and development of drugs that bind transferrin with high affinity.