Models for evaluating glioblastoma invasion along white matter tracts.

White matter tracts (WMs) are one of the main invasion paths of glioblastoma multiforme (GBM). The lack of ideal research models hinders our understanding of the details and mechanisms of GBM invasion along WMs. To date, many potential in vitro models have been reported; nerve fiber culture models and nanomaterial models are biocompatible, and the former have electrically active neurons. Brain slice culture models, organoid models, and microfluidic chip models can simulate the real brain and tumor microenvironment (TME), which contains a variety of cell types. These models are closer to the real in vivo environment and are helpful for further studying not only invasion along WMs by GBM, but also perineural invasion and brain metastasis by solid tumors.

Anionic Porous Zn-Metalated Porphyrin Metal-Organic Framework with PtS Topology for Gas-Phase Photocatalytic CO2 Reduction.

Presented here are the synthesis and gas-phase photocatalytic CO2 reduction of an anionic porous Zn-metalated porphyrin metal-organic framework (MOF) induced by an ionic liquid. The desired CO2 affinity and deep conduction band position of the MOF catalyst provide strong kinetic and thermodynamic advantages for photocatalytic CO2 to CH4 conversion with high selectivity (∼70%) in H2O vapor.

Isolating Fe-O2 Intermediates in Dioxygen Activation by Iron Porphyrin Complexes.

Dioxygen (O2) is an environmentally benign and abundant oxidant whose utilization is of great interest in the design of bioinspired synthetic catalytic oxidation systems to reduce energy consumption. However, it is unfortunate that utilization of O2 is a significant challenge because of the thermodynamic stability of O2 in its triplet ground state. Nevertheless, nature is able to overcome the spin state barrier using enzymes, which contain transition metals with unpaired d-electrons facilitating the activation of O2 by metal coordination. This inspires bioinorganic chemists to synthesize biomimetic small-molecule iron porphyrin complexes to carry out the O2 activation, wherein Fe-O2 species have been implicated as the key reactive intermediates. In recent years, a number of Fe-O2 intermediates have been synthesized by activating O2 at iron centers supported on porphyrin ligands. In this review, we focus on a few examples of these advances with emphasis in each case on the particular design of iron porphyrin complexes and particular reaction environments to stabilize and isolate metal-O2 intermediates in dioxygen activation, which will provide clues to elucidate structures of reactive intermediates and mechanistic insights in biological processes.

High loading of Mn(ii)-metalated porphyrin in a MOF for photocatalytic CO2 reduction in gas-solid conditions.

A high loading of Mn(ii)-metalated porphyrin was achievable in a 2D porphyrin-based Mn-MOF induced by an ionic liquid. The excellent stability, sufficient redox potential, atomically dispersed porphyrin Mn(ii) sites, desired CO2 affinity, high visible light-harvesting and efficient charge separation, endow this MOF with the overall photocatalytic conversion of CO2 to CH4 in gas-solid conditions.

Ionic liquid induced highly dense assembly of porphyrin in MOF nanosheets for photodynamic therapy.

Two-dimensional (2D) metal-organic framework (MOF) nanosheets have emerged as a new member of 2D nanomaterials for molecular sieving, energy conversion and storage, catalysis and biomedicine. In this paper, a highly dense assembly of porphyrin achievable in porphyrin-integrated MOF nanosheets induced by an ionic liquid is obtained by sonication exfoliation of its bulk crystals. The 2D layered structure MOF, [BMI]2[Ca3(H2TCPP)2(µ2-OH2)2(H2O)2] (1), was firstly prepared by using the ionic liquid assisted synthetic method (H6TCPP = meso-tetra(carboxyphenyl) porphyrin, BMI = 1-butyl-3-methylimidazolium). The laminated layers in 1 clearly indicate a weak interlayer non-covalent interaction but a strong metal-carboxylate bonding within the layers, which facilitates the exfoliation of 1 to form 2D MOF nanosheets (1 NSs). Powder X-ray diffraction (PXRD), high-resolution transmission electron microscopy (HR-TEM) and fast Fourier transform (FFT) patterns revealed that 1 NSs could maintain their crystalline structure after exfoliation. These MOF nanosheets exhibited excellent aqueous dispersibility, biodegradability and high cytotoxicity under light irradiation against MCF-7 cells.

Schisandrin B Improves the Renal Function of IgA Nephropathy Rats Through Inhibition of the NF-κB Signalling Pathway.

Schisandrin B (SchB) is an active compound extracted from the Chinese herb Schisandra chinensis and shows excellent anti-inflammatory activity. This study was performed to examine the effects of SchB in a rat model of IgA nephropathy (IgAN). IgAN was established in Sprague-Dawley rats by immunization with lipopolysaccharide (LPS), bovine serum albumin, and carbon tetrachloride. Renal function was evaluated by determining the levels of urinary red blood cells, proteinuria, blood urea nitrogen (BUN), and creatinine (Cr). Renal tissue and protein samples were collected for further analysis. Pre-treatment and treatment with SchB significantly ameliorated renal function of IgAN rats, which was evidenced by decreased levels of proteinuria, hematuria, BUN, and Cr. IgAN rats exhibited increased serum IgA, renal IgA deposition, mesangial cell proliferation, and inflammatory cell infiltration, which were significantly attenuated by intervention with SchB. Moreover, SchB inhibited infiltration of CD3+ and CD11b+ cells, decreased levels of tumour necrosis factor-alpha, interleukin-1ß, and monocyte chemoattractant protein-1 in the kidney, and decreased the numbers of CD3+CD69+ cells in the spleen. Of note, SchB therapy significantly increased cytoplasmic p65 and IκB expression and decreased nuclear p65 levels both in the damaged renal tissue and LPS-stimulated HK-2 cells, indicating a direct inhibitory effect on the NF-κB pathway in IgAN rats. Taken together, our data provide insight into a new application of SchB for the treatment of IgAN and represent a novel mechanism behind these effects.

A Microfluidic Strategy for Controllable Generation of Water-in-Water Droplets as Biocompatible Microcarriers.

Droplet microfluidics has been widely applied in functional microparticles fabricating, tissue engineering, and drug screening due to its high throughput and great controllability. However, most of the current droplet microfluidics are dependent on water-in-oil (W/O) systems, which involve organic reagents, thus limiting their broader biological applications. In this work, a new microfluidic strategy is described for controllable and high-throughput generation of monodispersed water-in-water (W/W) droplets. Solutions of polyethylene glycol and dextran are used as continuous and dispersed phases, respectively, without any organic reagents or surfactants. The size of W/W droplets can be precisely adjusted by changing the flow rate of dispersed and continuous phases and the valve switch cycle. In addition, uniform cell-laden microgels are fabricated by introducing the alginate component and rat pancreatic islet (ß-TC6) cell suspension to the dispersed phase. The encapsulated islet cells retain high viability and the function of insulin secretion after cultivation for 7 days. The high-throughput droplet microfluidic system with high biocompatibility is stable, controllable, and flexible, which can boost various chemical and biological applications, such as bio-oriented microparticles synthesizing, microcarriers fabricating, tissue engineering, etc.

[Interventional effects of emodin on transforming growth factor-beta1/integrin-linked kinase signal way in interleukin-1beta-induced transdifferentiation of rat tubular epithelial-myofibroblasts].

OBJECTIVE: To study the effects of transforming growth factor-beta1/integrin-linked kinase (TGF-beta1/ILK) signal way in interleukin-1beta (IL-1beta)-induced rat tubular epithelial-myofibroblast transdifferentiation (TEMT), and to investigate whether emodin inhibits IL-1beta-induced TEMT through the TGF-beta1/ILK signal way-dependent mechanism. METHODS: Normal rat kidney epithelial cell line (NRK52E) was used in this study. NRK52E cells were divided into blank control group, emodin control group, IL-1beta-induced group, emodin-inhibited group, SB431542 (TGF-beta 1 type I receptor blocker)-inhibited group, emodin plus SB431542-inhibited group, emodin-pretreated group and emodin-reversed group. After 48-hour culture, morphological changes of the NRK52E cells were observed by an inverted phase contrast microscope. The expressions of alpha-smooth muscle actin (alpha-SMA) and E-cadherin were detected by two-color immunohistochemical staining, while the expressions of TGF-beta1 and ILK were detected by one-color immunohistochemical staining. We also performed the imaging analysis to quantitatively analyze the result of the immunohistochemical staining. The secretion of fibronectin (FN) was analyzed by enzyme-linked immunosorbent assay. RESULTS: Compared with the blank control group, IL-1beta might induce TEMT, which was showed in increasing expression of alpha-SMA, increasing secreting of FN and decreasing expression of E-cadherin, and at the same time the expressions of TGF-beta1 and ILK were enhanced (P<0.05). Emodin might inhibit all of those changes induced by IL-1beta (P<0.05). When TGF-beta1 signal way was intercepted, IL-1beta induced-TEMT was suppressed and the expression of ILK was decreased, however, there was no significant difference in expression of TGF-beta1 between the SB431542 group and the IL-1beta-induced group. Compared with emodin-inhibited group, emodin-pretreatment could not prevent IL-1beta induced-TEMT in a certain extent, but emodin could not revert IL-1beta-induced TEMT. Spearman correlation analysis showed that TGF-beta1 expression had positive correlation with expressions of alpha-SMA, FN, ILK and negative correlation with E-cadherin expression, and the expression of ILK was positively correlated with the expressions of alpha-SMA and FN and negatively correlated with E-cadherin expression. CONCLUSION: IL-1beta induces TEMT partly depending on TGF-beta1/ILK signal way, partly via which emodin inhibits the TEMT induced by IL-1beta.

2-Iodo-1,3-dimethoxy-benzene.

Crystals of the title compound, C(8)H(9)IO(2), were obtained from a dimethyl sulfoxide solution of 2,6-dimethoxy-benzoic acid and iodo-benzene diacetate under a nitro-gen atmosphere at 353 K. In the crystal structure, mol-ecules are linked by weak C-H⋯π inter-actions, generating inter-penetrating one-dimensional chains of perpendicularly oriented mol-ecules extending along [011] and [01]. Chains are also formed through non-bonding C-I⋯π contacts extending in the same directions, projecting a zigzag motif in view down [100]. The I⋯Cg distance is 3.695 (2) Šand the C-I⋯Cg angle is 164.17 (14)°. The mol-ecular symmetry m coincides with the mirror plane of the space group Cmc2(1), resulting in a half-mol-ecule in the asymmetric unit (Z' = ½).

[Interventional effect of emodin on the expression of intergern linked kinase in tubular epithelial-myofibroblast transdifferentiation].

AIM: To observe the change of ILK expression in interleukin-1beta(IL-1beta)-induced tubular epithelial-myofibroblast transdifferentiation, and to investigate whether emodin inhibit IL-1beta-induced tubular epithelial-myofibroblast transdifferentiation through an intergern linked kinase-dependent mechanism. METHODS: Normal rat kidney epithelial cell line (NRK52E) was cultured and then divided into blank group, emodin control group, IL-1beta-induced group and emodin-inhibited group. When the cells were cultured for 48 h, their morphological changes were observed by an inverted phase contrast microscope. The expression of a-smooth muscle actin (a-SMA) and E-cadherin were detected using a two-color immunohistochemistry staining technique, while the expression of integrin-linked kinase (ILK) was detected using a one-color immunohistochemistry staining technique. The secretion of fibronectin (FN) was analyzed by ELISA. RESULTS: NRK52E cells cultured with IL-1 became fibroblast-like in appearance. The expression of a-SMA was enhanced (65h5+/-1h7 vs 140h4+/-3h0, P<0h05), the expression of E-cadherin was decreased (82h5+/-1h0 vs 36h0+/-2h8, P<0h05), the expression of ILK was enhanced (36h1+/-3h1 vs 82h4+/-1h2, P<0h05), and the secretion of FN was increased (54h6+/-3h1 vs 124h8+/-3h2 mg/L, P<0h05). Emodin markedly inhibited all of those changes induced by IL-1beta. CONCLUSION: The expression of ILK is up-regulated in IL-1beta-induced tubular epithelial-myofibroblast transdifferentiation. Emodin might inhibit TEMT by a down-regulation the expression of ILK.

1,3-Di-4-pyrid-ylpropane-2-hydroxy-benzene-1,4-dicarboxylic acid (1/2).

In the title compound, C(13)H(14)N(2)·2C(8)H(6)O(5), which crystallized in the monoclinic C2/c space group, the 1,3-bis-(4-pyrid-yl)propane mol-ecules and 2-hydr-oxy-1,4-benzene-dicarboxylic acid mol-ecules are alternately linked by O-H⋯N and O-H⋯O hydrogen bonds into herringbone/zigzag chains.