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To solve the biofouling problem of polyvinyl alcohol (PVA) hydrogel as the artificial cornea, glycidyl methacrylate (GMA) and 2-hydroxypropyltrimethyl ammonium chloride chitosan (HACC) were grafted on the surface of PVA hydrogel via a new method of photoinduced electron transfer—reversible addition fragmentation chain transfer (PET-RAFT) polymerization and ring-open reaction. Both attenuated total reflectance Fourier transform infrared spectroscopy (ATR-FTIR), X-ray photoelectron spectroscopy (XPS), atomic force microscopy (AFM), scanning electron microscope (SEM), and thermogravimetric analysis (TGA) confirmed that GMA and HACC were successfully grafted on the surface of PVA hydrogel. A series of experiments to test the hydrophilicity of PVA hydrogel showed that it became hydrophobic due to the introduction of hydrophobic groups after grafting with GMA and HACC. In addition, cytotoxicity in vitro of PVA-g-p(GMA-HACC) hydrogel could be considered as not cytotoxicity according to ISO 10993-5: 2009. The anti-fouling property of hydrogel decreased after grafting with GMA due to the hydrophobic surface, while increased after grafting with HACC due to the steric repulsion of p(GMA-HACC) polymer brush. It’s no doubt that PET-RAFT was a feasible and reliable surface modification method which could be used in many biomolecules due to the excellent advantages.

Bisphenol A (BPA) is an environmental oestrogen or xenoestrogen (XEs). XEs represent a health risk due to their potential for endocrine disruption and ability to mimic estrogenic activity. The effects of BPA on isolated hearts under normal and ischemia/reperfusion (I/R) conditions were investigated for the first time, with a focus on the effects of BPA and 17β-oestradiol (E2) co-administration on I/R injury. Our results indicated that BPA at 10−7 M and 10−5 M did not significantly affect heart rate (HR), coronary flow (CF), lactate dehydrogenase (LDH) or creatine kinase (CK) release in normal or I/R isolated hearts within the 90 min. However, E2 exerted a protective effect against I/R injury, whereas, BPA inhibited the cardio-protective effects of E2 on HR, CF, and LDH and CK release. Furthermore, BPA in combination with E2 aggravated I/R injury by increasing infarct size and causing a more severe ultrastructural disruption as compared to treatment with E2 alone. Based on our results, we conclude that BPA inhibits the cardio-protective effects of E2 on I/R-injured hearts, despite not significantly affecting normal or I/R isolated hearts.

In this study, we grafted brush-like CBMA copolymer brushes onto the surface of PVA hydrogel membrane through photo-induced electron transfer–reversible addition fragmentation chain transfer (PET-RAFT) polymerization. ATR-FTIR, XPS, AFM, UV–Vis absorption spectra and elemental analysis were adopted to characterize the hydrogels, and equilibrium swelling, water contact angle, vitro cytotoxicity assay, protein adsorption and cells adhesion experiments were used to evaluate the related property of hydrogels. The results of ATR-FTIR and XPS showed that pCBMA was successfully grafted onto the surface of PVA hydrogel membrane. The Ra roughness of hydrogel surface in AFM increased slightly from 5.44 nm to 6.12 nm. Transmittance of the PVA-g-pCBMA hydrogel in the visible range (380 nm-780 nm) was remaining at 91.2%–97.0%. The optimal reaction conditions (CPADB: 1.20 mmol/L, Eosin Y: 0.03 mmol/L and CBMA: 358 mmol/L) were confirmed through control experiments. The equilibrium swelling and water contact angle showed that the swelling ratio increased from 2.06 cm3 g−1 to 3.65 cm3 g−1, while the water contact angle decreased from 45.94° to 18.06° with the increase of grafting ratio (23.92%–55.18%). In vitro cytotoxicity assay by CCK-8 showed that the cells relative viability remained at least 90.55%. Anti-protein adsorption experiment illustrated approximately 57.2% improvement of anti-protein capacity at 37 °C, while cells adhesion experiment also showed about 64.57% improvement of anti-cells capacity. These results revealed the applicability of the oxygen tolerant PET-RAFT mechanism on the PVA modification and it was effective, feasible and non-cytotoxic method to prepare the other functional PVA hydrogel membrane.

A novel g-C3N4@InVO4 semiconductor catalyzed surface-initiated photo atom transfer radical polymerization without catalysts residues problem has been developed. This method proceeded in N-methyl pyrrolidone/aqueous under atmospheric conditions. To verify the versatility of this method and enhance the antifouling properties of polyvinyl alcohol (PVA) hydrogel, two types of fluorinated polymer brushes (p6F/p13F) were successfully constructed on PVA hydrogel surface instead of the subsurface. The chemical bonds between PVA matrix and fluorinated polymer brushes (p6F/p13F) enhanced the surface cross link density and resulted in an increase of thermal stability and mechanical properties. All fluorinated PVA hydrogels with excellent antifouling properties was able to tackle the biofouling problem in complex environment of the human body. In addition, all fluorinated PVA hydrogels was no cytotoxicity for L929 and NDHF according to ISO 10993.5:2009. g-C3N4@InVO4 catalyzed SI-photoATRP provides a novel surface modification technology for various biological or medical materials in the industrial-scale application.

An innovative g-C3N4 catalyzed surface-initiated photo atom transfer radical polymerization (SI-photoATRP) has been developed to construct MEDSAH zwitterionic polymer brushes on PVA hydrogel surface. g-C3N4 catalyzed SI-photoATRP is temporal and spatial control. As a heterogeneous reaction system, it can solve the catalyst residues problem. After grafting with MEDSAH, surface chemical composition and morphology of PVA-g-pMEDSAH hydrogel confirmed that MEDSAH was successfully grafted onto PVA hydrogel. Thermal property of PVA-g-pMEDSAH hydrogel decreased and hydrophilicity increased. No statistically significant differences between PVA and PVA-g-pMEDSAH were observed on mechanical properties. Cytotoxicity in vitro of PVA-g-pMEDSAH hydrogel could be considered as no cytotoxicity for L929 and NDHF cells. The antifouling properties of PVA-g-pMEDSAH hydrogel were significantly improved due to the enhancement of the surface hydration and steric repulsion effects caused by pMEDSAH polymer brushes. In addition, g-C3N4 is easier to modify to enhance the photocatalyst property. Thus, the heterogeneous reaction system of g-C3N4 catalyzed SI-photoATRP has huge potential applied in biomaterials surface modification.

Astragaloside IV (AS-IV) is one of the active ingredients in Astragalus membrananceus (Huangqi), a traditional Chinese medicine. The present study investigated the effects of AS-IV on Ca[Formula: see text] handling in cardiac myocytes to elucidate its possible mechanism in the treatment of cardiac disease. The results showed that AS-IV at 1 and 10[Formula: see text][Formula: see text]M reduced KCl-induced [Ca[Formula: see text]]i increase ([Formula: see text] from 1.33[Formula: see text][Formula: see text][Formula: see text]0.04 (control, [Formula: see text] 28) to 1.22[Formula: see text][Formula: see text][Formula: see text]0.02 ([Formula: see text], [Formula: see text] 29) and 1.22[Formula: see text][Formula: see text][Formula: see text]0.02 ([Formula: see text] 0.01, [Formula: see text]), but it enhanced Ca[Formula: see text] release from SR ([Formula: see text] from 1.04[Formula: see text][Formula: see text][Formula: see text]0.01 (control, [Formula: see text]) to 1.44[Formula: see text][Formula: see text][Formula: see text]0.03 ([Formula: see text], [Formula: see text]) and 1.60[Formula: see text][Formula: see text][Formula: see text]0.04 ([Formula: see text] 0.01, [Formula: see text]0), in H9c2 cells. Similar results were obtained in native cardiomyocytes. AS-IV at 1 and 10[Formula: see text][Formula: see text]M inhibited L-type Ca[Formula: see text] current ([Formula: see text] from [Formula: see text]4.42[Formula: see text][Formula: see text][Formula: see text]0.58 pA/pF of control to [Formula: see text]2.25[Formula: see text][Formula: see text][Formula: see text]0.12 pA/pF ([Formula: see text] 0.01, [Formula: see text] 5) and [Formula: see text]1.78[Formula: see text][Formula: see text][Formula: see text]0.28 pA/pF ([Formula: see text] 0.01, [Formula: see text] 5) respectively, when the interference of [Ca[Formula: see text]]i was eliminated due to the depletion of SR Ca[Formula: see text] store by thapsigargin, an inhibitor of Ca[Formula: see text] ATPase. Moreover, when BAPTA, a rapid Ca[Formula: see text] chelator, was used, CDI (Ca[Formula: see text]-dependent inactivation) of [Formula: see text] was eliminated, and the inhibitory effects of AS-IV on ICaL were significantly reduced at the same time. These results suggest that AS-IV affects Ca[Formula: see text] homeostasis through two opposite pathways: inhibition of Ca[Formula: see text] influx through L-type Ca[Formula: see text] channel, and promotion of Ca[Formula: see text] release from SR.

Design of artificial corneal scaffolds substitute is crucial for replacement of impaired cornea. In this paper, porous polyvinyl alcohol/silk fibroin/nano-hydroxyapatite (PVA/SF/n-HA) composite hydrogel was prepared via the genipin (GP) cross-linking, the pore diameter of the hydrogel ranged from 8.138 nm and 90.269 nm, and the physical and physiological function of hydrogel were investigated. The resulting hydrogel exhibited favourable physical properties. With the GP content increasing, the structural regularity of PVA/SF/n-HA composite hydrogel was enhanced and the thermal stability was improved. The moisture content was slightly decreased and generally maintained at approximately 70%. The tensile strength was heightened up to 0.64 MPa, while the breaking elongation was decreased slightly. Moreover, the biofunction was investigated. The

N-methyl berbamine (N-MB) is a berberine derivative. Its analogue berbamine has been reported to have remarkable antiarrhythmic and ischemic protective effects. However, the pharmacological effects of N-MB are ill-defined. In this study, molecular docking was used to evaluate the binding of N-MB to CaV1.2 Ca2+ and KV11.1 K+ channels, and the effects of N-MB on action potential and ionic currents were observed in the ventricular myocytes of rabbits, HEK293 cells stably transfected with the hCaV1.2 gene and CHO cells stably transfected with hERG (human ether-a-go-go related gene). The results showed that N-MB was able to bind to both CaV1.2 and KV11.1 channels. Following a perfusion with N-MB, the durations of action potentials (APD20, APD50 and APD90) were extended, and the outward tail current, Itail, as well as the hERG current, IhERG, were inhibited, while the amplitude of action potential (APA) was only slightly reduced. N-MB also decreased the peak amplitude of the L-type Ca2+ channel current, ICaL, as well as the CaV1.2 current, ICaV1.2; this may limit the prolongation of APD. In conclusion, N-MB is a potent and natural antiarrhythmic multitarget drug that may elicit its antiarrhythmic effect through blocking both Ca2+ and K+ channel currents. Keywords: N-methyl berbamine, Action potential, Ca2+ current, K+ current, Multitarget

PVA was dissolved in mixed solvent (DMSO and water) and followed by several freeze-thaw cycles in a mold to produce PVA membrane. Surface modification of PVA membranes by HA molecules was investigated to improve the hydrophilicity of the membrane surface thereby reducing adsorption of the proteins onto the membrane. The surface composition, water contact angle, optical and mechanical properties, surface morphology, cell compatibility and protein adhesion were systematically investigated. ATR-FTIR spectra, XPS, SEM and AFM indicated that PVA membranes were successfully modified by grafting of the HA. The modified membranes showed increased hydrophilicity and cytocompatibility, decreased surface roughness and mechanical properties, and suppressed cell and protein adhesion compared to the pristine membrane. In general, the achievement of the HA coating with anti-adhesive property can potentially be widely used on surface modification of artificial cornea and other biomedical implants.

Nonylphenol (NP) is one of the widely spread xenoestrogens (XEs) and is used in the production of industrial and consumer surfactants. In the present study, we examined the acute effects of NP on myocardial contractility to determine its rapid-response cardiac effects in the isolated heart. We also investigated the mechanism of action of NP by determining its effects on the L-type Ca(2+) channel (LTCC) currents (ICa-L) in ventricular myocytes. Lower concentrations (10(-12)-10(-10)M) of NP increased cardiac contractility while higher concentrations (10(-8)-10(-6)M) exhibited opposite effects. These apparently opposing effects suggest that NP has biphasic concentration-dependent rapid effects on cardiac contractility. These non-monotonic changes in contractility correlated with the effects of NP on ICa-L, indicating that ion channels, as rapidly responding membrane proteins, play a very important role in mediating the rapid-response effects of XEs. Further studies revealed that the G protein coupled receptor 30 (GPR30) mediates the effects of NP on LTCC at lower but not higher concentrations, implying that the differential involvement of GPR30 might be responsible for the non-monotonic effects of NP.

We have investigated the characteristics of voltage-gated K+ channels and L-type Ca2+ channels in GH3 rat pituitary cells and the effects of the xenoestrogen (XEs) nonylphenol (NP) on these ion channel currents. Our results have shown that the lower concentrations (10−15–10−14 M) of NP decreased the amplitudes of voltage-gated K+ currents (IKv) and activated L-type Ca2+ currents (ICa-L) by reducing half-activation membrane potentials of activation kinetics curves. However, the higher concentrations (10−10–10−9 M) of NP increased the amplitudes of IKv and inhibited ICa-L by reducing the peak values of ICa-L. Thus, NP affects IKv and ICa-L in an opposite and non-monotonic manner.

Nonylphenol (NP), a widely distributed, toxic, endocrine-disrupting chemical, has estrogenic properties. However, its cardiac effects remain unclear. In this study, the effects of NP on isolated guinea pig hearts were studied in three separate experiments. First, hearts were perfused with 10⁻⁷ M NP or 10⁻⁵ M NP to determine whether NP was toxic to isolated healthy hearts. Next, hearts were subjected to 50 min of ischemia and 60 min of reperfusion (I50R60) with 10⁻⁷ M NP or 10⁻⁵ M NP to determine whether NP could aggravate ischemia/reperfusion (I/R) injury. Finally, the interaction of the cardio-protective agent 17β-estradiol (E₂) with NP was studied using 10⁻⁷ M E₂, 10⁻⁷ M E₂ plus 10⁻⁷ M NP, and 10⁻⁷ M E₂ plus 10⁻⁵ M NP. Heart rate (HR) and coronary flow (CF) were significantly decreased and the leakage of lactate dehydrogenase (LDH) in effluent was increased in the 10⁻⁵ M NP group. However, there were no obvious changes in HR, CF, the leakage of LDH or creatine kinase (CK), or the activity of superoxide dismutase in either of the NP treatments in the I50R60 model. Treatment with 10⁻⁷ M E₂ attenuated I/R injury by increasing HR, decreasing the leakage of LDH and CK, and decreasing infarct size. However, these effects were reversed by both concentrations of NP. These data demonstrate that NP had direct toxic effects on normal hearts and NP might disrupt the cardio-protective effects of E₂ on I/R injury.

Survivin, which is a member of the inhibitor of apoptosis protein family, was found originally in immature cells and cancer cells but not in non-neoplastic adult tissues. The subsequent identification of four other alternative splice variants that possess distinct functions and localizations suggested the diverse roles of survivin isoforms. An unspecified isoform of survivin was found recently to be induced in terminally differentiated neutrophils by cytokines that prolong the neutrophil lifespan, such as GM-CSF and G-CSF, suggesting the importance of survivin in blocking apoptosis in neutrophils. To examine the mechanism by which survivin inhibits neutrophil apoptosis, we attempted to induce survivin by GM-CSF/G-CSF in an HL60 cell line that was differentiated into neutrophils by all-trans retinoic acid and DMSO and freshly isolated human neutrophils. The antiapoptotic isoform “Survivin,” which was decreased during differentiation, was re-induced by GM-CSF in neutrophil-like, differentiated HL60. In contrast, in normal neutrophils, survivin mRNA was observed to increase spontaneously after 24 h incubation, and no additional elevation was induced by GM-CSF/G-CSF, which exerted their antiapoptotic effects on the neutrophils in 6 h, despite the lack of survivin induction. PCR and Western blotting detected Survivin-2α, a dominant-negative of antiapoptotic Survivin, with no other isoforms in the freshly isolated or incubated neutrophils. Our study revealed that the expressed isoforms and the response to GM-CSF were different between the HL60-derived and normal neutrophils, which predominantly expressed Survivin-2α, not likely involved in apoptosis inhibition by GM-CSF/G-CSF.