Simultaneous fractionation of multiple classes of polyphenols from honeybush tea using solid-phase extraction

The structural diversity of polyphenols and the inherent limitations of current extraction techniques pose a challenge to extract polyphenols using a simple and green method. Hence, in this study, a method was developed to simultaneously fractionate multiple classes of polyphenols by only varying ethanol-water solutions. Honeybush tea, which is rich in polyphenols, was selected as a model for this study. Solvent extraction followed by solid-phase extraction (SPE) was developed to obtain a polyphenol-rich fraction from six honeybush samples. Based on a gradient elution programme (10%, 30%, 50%, 70% and 90% (v/v) ethanol-water solution) of SPE, the Strata X cartridge showed a better recovery of most targeted polyphenols under 0.9 mL of the drying volume and 1 mL min⁻¹ of the dispensing speed. The elution programme for fractionating most polyphenols was as follows: single elution with 50% ethanol, followed by twice elution with 70% ethanol. The antioxidant capacity was used to analyse the differences among the polyphenol-rich fractions from six honeybush samples. Principal component analysis (PCA) revealed that unfermented C. genistoides (GG) has the greatest antioxidant capacity among the honeybush species studied. Additionally, mangiferin, isomangiferin and vicenin-2 were the main contributors to the antioxidant capacity in six honeybush fractions according to the correlation study.     

Ferulic acid and EGCG alter the structural characteristics of ovalbumin and its application in mineral loading

This study aims to fabricate mineral-loading nanocarriers using natural materials. The interaction patterns between ovalbumin (OVA) and four water-soluble polyphenols, namely ferulic acid (FA), (-)-Epigallo-catechin 3-gallate (EGCG), gallic acid (GA) and epicatechin (EC), were investigated. Results showed that the optimised conditions for preparing stable OVA–polyphenol complexes are at the OVA–polyphenol ratio of 4:1 at pH 6, under which OVA–FA and OVA–EGCG showed the highest stability and mineral-loading capacity among four OVA–polyphenol complexes. The fluorescence results indicated that the addition of EGCG and FA induced a significant fluorescence quenching to OVA. The interaction between OVA and polyphenols involved hydrogen bonding, hydrophobic interaction and electrostatic interaction. Fourier transform infrared spectroscopy (FTIR) analysis suggested that both FA and EGCG enhanced the stability and orderliness of the structure of OVA. The transmission electron microscopy images also exhibited the spherical structure of OVA after the addition of FA and EGCG. Furthermore, scanning electron microscope–energy dispersive X-ray spectrum results suggested that OVA–FA and OVA–EGCG complexes were better mineral carriers than OVA–GA and OVA–EC. This study may serve as the theoretical support for the promising application of OVA in the fabrication of mineral-loading nanocarriers in functional food and pharmaceutic.     

ROS-Mediated Anti-Tumor Effect of Coptidis Rhizoma against Human Hepatocellular Carcinoma Hep3B Cells and Xenografts

Coptidis Rhizoma is the dried rhizome from the Coptis chinensis Franch. that has been shown to have a number of beneficial pharmacological properties including antioxidant, anti-inflammatory, and anti-cancer effects. However, the anti-cancer effects of Coptidis Rhizoma on hepatocellular carcinoma (HCC) remain unclear. In this study, we investigated the anti-cancer properties of Coptidis Rhizoma ethanol extract (CR) in HCC Hep3B cells and in a xenograft mouse model. Our results showed that the CR significantly inhibited cell growth and induced apoptosis in Hep3B cells through increased expression of Bcl-2 associated x-protein (Bax) and cleavage of poly-ADP ribose polymerase (PARP), reduced expression of Bcl-2, and activated caspases. CR also increased the generation of intracellular reactive oxygen species (ROS), which caused a loss of mitochondrial membrane potential (MMP, ΔΨm) and activation of the mitochondria-mediated intrinsic apoptosis pathway. Moreover, N-acetylcysteine (NAC), a ROS inhibitor, markedly blocked the effects of CR on apoptotic pathways. CR also induced the expression of light chain 3 (LC3)-I/II, a key autophagy regulator, whereas CR-mediated autophagy was significantly suppressed by NAC. In addition, pre-treatment with NAC perfectly attenuated the inhibition of cell invasion and migration of CR-stimulated Hep3B cells. Furthermore, oral administration of CR suppressed Hep3B tumor growth in xenograft mice without toxicity, alterations to body weight, or changes in hematological and biochemical profiles. Taken together, our findings suggest that CR has anti-tumor effects that result from ROS generation, and may be a potential pharmacological intervention for HCC.     

Nb2O5-doped NiZnCo ferrite ceramics with ultra-high magnetic quality factor and low coercivity for high-frequency electronic devices

This work investigates the influence of niobium pentoxide (Nb₂O₅) as dopant, on the structural, magnetic, and dielectric properties of NiZnCo ferrites. The results showed that Nb₂O₅ was an effective dopant, and the Nb⁵⁺ ions entered the B site to replace Fe³⁺ ions, which altered the electromagnetic properties of the NiZnCo ferrite. In particular, the coercivity (H_c) was 20～24 Oe, and the magnetic quality factor (Q), was more than 200 at x = 0 and x = 0.1 wt%, which is 4～5 times higher than that of NiZn and NiCuZn ferrites. Excellent electromagnetic properties were obtained for 0.1 wt% Nb₂O₅-doped NiZnCo ferrite, i.e., M_s = 88.3 emu/g, H_c =20.4 Oe, ρ = 2.4 × 10⁵ Ω m and Q = 202 @20 MHz. These excellent electromagnetic properties of Nb₂O₅-doped NiZnCo ferrites could be potentially applied to resonators and capacitors at high frequency.     

Influence of fluorine-containing side chain on the properties of waterborne polyurethane-urea

In order to prepare waterborne polyurethane with excellent water resistance and thermodynamic properties, a series of side chain fluorinated waterborne polyurethane-urea (FWPU-UA) was synthesized with polytetramethylene ether glycol, N-(2-methyl-1,3-propanediol-2′-)-perfluoro-1-butanesulfonyl amine (NPBA), isophorone diisocyanate, and isophoronediamine. With the increase of NPBA content, the weight loss temperature, glass transition temperature, and tensile strength of FWPU-UA were all improved. Gaussian fitting analysis of infrared data and density functional theory simulation proved that the introduction of fluorine side chains increased the interaction of hydrogen bonding in the FWPU-UA. X-ray photoelectron spectroscopy analysis indicated that the aggregation of fluorine atoms on the surface of film were caused by the migration and enrichment of fluorine side chains. Furthermore, the water resistance of polyurethane-urea film could be significantly improved by adding a small amount of NPBA, and the seven-day water absorption rate of polyurethane-urea film was reduced from 30.13% to 12.55%.     

4-Methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene,a Major Active Metabolite of Bisphenol A,Triggers Pancreatic β-Cell Death via a JNK/AMPKα Activation-Regulated Endoplasmic Reticulum Stress-Mediated Apoptotic Pathway

4-methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene (MBP), a major active metabolite of bisphenol A (BPA), is generated in the mammalian liver. Some studies have suggested that MBP exerts greater toxicity than BPA. However, the mechanism underlying MBP-induced pancreatic β-cell cytotoxicity remains largely unclear. This study demonstrated the cytotoxicity of MBP in pancreatic β-cells and elucidated the cellular mechanism involved in MBP-induced β-cell death. Our results showed that MBP exposure significantly reduced cell viability, caused insulin secretion dysfunction, and induced apoptotic events including increased caspase-3 activity and the expression of active forms of caspase-3/-7/-9 and PARP protein. In addition, MBP triggered endoplasmic reticulum (ER) stress, as indicated by the upregulation of GRP 78, CHOP, and cleaved caspase-12 proteins. Pretreatment with 4-phenylbutyric acid (4-PBA; a pharmacological inhibitor of ER stress) markedly reversed MBP-induced ER stress and apoptosis-related signals. Furthermore, exposure to MBP significantly induced the protein phosphorylation of JNK and AMP-activated protein kinase (AMPK)α. Pretreatment of β-cells with pharmacological inhibitors for JNK (SP600125) and AMPK (compound C), respectively, effectively abrogated the MBP-induced apoptosis-related signals. Both JNK and AMPK inhibitors also suppressed the MBP-induced activation of JNK and AMPKα and of each other. In conclusion, these findings suggest that MBP exposure exerts cytotoxicity on β-cells via the interdependent activation of JNK and AMPKα, which regulates the downstream apoptotic signaling pathway.     

Activation of the Complement System on Human Endothelial Cells by Urban Particulate Matter Triggers Inflammation-Related Protein Production

Exposure to particulate matter (PM) is becoming a major global health issue. The amount and time of exposure to PM are known to be closely associated with cardiovascular diseases. However, the mechanism through which PM affects the vascular system is still not clear. Endothelial cells line the interior surface of blood vessels and actively interact with plasma proteins, including the complement system. Unregulated complement activation caused by invaders, such as pollutants, may promote endothelial inflammation. In the present study, we sought to investigate whether urban PM (UPM) acts on the endothelial environment via the complement system. UPM-treated human endothelial cells with normal human serum showed the deposition of membrane attack complexes (MACs) on the cell surface via the alternative pathway of the complement system. Despite the formation of MACs, cell death was not observed, and cell proliferation was increased in UPM-mediated complement activation. Furthermore, complement activation on endothelial cells stimulated the production of inflammation-related proteins. Our results revealed that UPM could activate the complement system in human endothelial cells and that complement activation regulated inflammatory reaction in microenvironment. These findings provide clues with regard to the role of the complement system in pathophysiologic events of vascular disease elicited by air pollution.