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PurposeMethodsResultsThis study explores the immune cells’ role in anti-VEGF resistance in nAMD patients, and the potential of Zi-Yin-Jiang-Huo-Tang (ZYJHT), a Traditional Chinese Medicine formula, as complementary therapy.Aqueous humor proteomics data from 10 nAMD patients with anti-VEGF resistance and 10 nAMD patients without anti-VEGF resistance were analyzed, investigating immune cells’s role in anti-VEGF resistance and its underlying mechanism. Network pharmacology methods are employed to analyze the active ingredients in ZYJHT that contribute to therapeutic effects and their mechanisms. Real-time PCR (polymerase chain reaction) was used to detect changes in the expression of SOD1 (superoxide dismutase 1) after treatment with compounds targeting SOD1 in ARPE-19 cells.nAMD patients with anti-VEGF resistance showed enhancement of biological processes linked to the positive regulation of immune function, along with decreased cellular resistance to oxidative stress. Infiltration of B cells memory, plasma cells, CD8+and γδ-T cells were higher in nAMD patients with anti-VEGF resistance. SOD1 was identified as a hub gene in the occurrence of anti-VEGF resistance and a core therapeutic target of ZYJHT, negatively correlated with B and T cell infiltration. Compounds diosgenin, naringenin, and liquiritin in ZYJHT can bind to SOD1 and upregulating SOD1 expression in ARPE-19 cells. [ABSTRACT FROM AUTHOR]

In this study, sesbania gum (SG) was successfully modified by using H2O2 as the oxidant, CuSO4 as the catalyst, and octenyl succinic anhydride as the esterification agent. The effects of oxidation and esterification on the structure and properties of SG were investigated by Fourier transform infrared spectroscopy (FTIR), X-ray diffraction (XRD), and thermogravimetric analysis (TGA), among other techniques. By FTIR analysis it was found that the oxidation did not introduce new groups, while the ester carbonyl group was successfully introduced into the molecular chain of SG. The oxidation of SG by H2O2 involves the cleavage of long chains, which is also the main cause of its reduction in viscosity. Oxidation reduced the crystallinity of SG, and its crystal structure was found to be severely damaged after esterification. Both oxidation and esterification altered the thermal properties of SG, whereby the thermal stability and freeze-thaw stability of the modified SG were improved and the expansion capacity was effectively reduced. [ABSTRACT FROM AUTHOR]

In this paper, the influence of negatively charged active fluorescent dextran on electrofusion of barley protoplasts was investigated. We discovered that this biopolymer inhibits the electrofusion process. The adsorption of fluorescent dextran on membranes was determined by observing their fluorescence microphotograph in protoplast suspension. A green fluorescent ring appeared around the membrane. The adsorption phenomena were also investigated by measuring the influence of additives on electrophoresis of protoplasts. It was detected that the membrane of barley protoplasts had a negative charge. After being stored in solution containing fluorescent dextran, the protoplasts demonstrated increased relative mobility due to the increase of negative charge on membranes by adsorption. The mobility decreased when the protoplasts were pretreated in the solution containing positively charged substances Bardac 2080. The increase of the membrane's negative charge by adsorption F-DX enhances the repulsion between protoplasts, and therefore decreases the electrofusion yield. [ABSTRACT FROM AUTHOR]

Emodin (1,3,8-trihydroxy-6-methylanthraquinone), a natural anthraquinone compound isolated from the rhizome of rhubarb, has been reported to treat brain injury after intracerebral hemorrhage. Treatment of neurons with emodin is able to decrease glutamate excitotoxicity, modulate calcium homeostasis, and induce Bcl-2 expression. However, the effects of emodin on the brain-resident innate immune cells are unclear. In the present study, the mouse microglial cell line, BV-2, was selected to investigate the effects of emodin on microglial activation and apoptosis. Cell viability and apoptosis were sequentially measured with the CellTiter-Glo Luminescent Cell Viability Assay, YOPRO-1 and Caspase-Glo 3/7 Assay Systems. The degree of microglial activation was evaluated using quantitative RT-PCR to measure expression of inflammatory markers. Treatment of BV-2 cells with emodin caused caspase-mediated apoptosis in a dose-dependent manner, and emodin augmented LPS-induced microglial apoptosis to repress inflammatory activation. In response to emodin treatment, reactive oxygen species (ROS) production was increased, and TRB3 was markedly activated. siRNA knockdown of TRB3 attenuated emodin-induced microglial apoptosis. Ectopic overexpression of TRB3 decreased cell viability and was associated with dysregulation of the prosurvival Akt/FOXO3 pathway. These results demonstrate that emodin induces BV-2 cell apoptosis through TRB3 and consequently eliminates inflammatory microglia. Our findings provide a novel molecular basis through which emodin exerts neuroprotective effects, treating brain injury after intracerebral hemorrhage. [ABSTRACT FROM AUTHOR]

Epidemiological studies have demonstrated that vitamin C decreases the risk of stroke, which has generally been ascribed to its function as antioxidant and free radical scavenger. However, whether there is a defined molecular target for vitamin C on stroke is unknown. Utilizing middle cerebral artery occlusion (MCAO) in rats as a model for ischemic stroke, we demonstrated that long-term, low-dose administration of vitamin C prior to MCAO could exert significant neuroprotective effect on the brain damage. The long-term, low-dose vitamin C pretreated rats had decreased brain infarct size and decreased neurological deficit score compared with the vehicle or single high dose pretreated MCAO rats. Furthermore, electrophysiological experiments using patch clamp technique showed that vitamin C increased the whole-cell current of the large-conductance Ca2+-activated K+ (BKCa) channel. Moreover, vitamin C increased the open probability of the channel without change its amplitude. Importantly, blockade of the BKCa channels abolished the neuroprotective effect of vitamin C on MCAO. Therefore, this study shows that long-term, low-dose pretreatment with vitamin C could reduce MCAO-induced brain damage through activation of the BKCa channels, suggesting that the BKCa channel is a molecular target of vitamin C on stroke. [ABSTRACT FROM AUTHOR]

MnOOH nanorods with rectangular cross-sections have been successfully prepared in high yield via a hydrothermal reduction process at a low temperature. After the subsequent heat treatment of the as-prepared MnOOH nanorods at 350°C for 6 h in air, β-MnO2nanorods with rectangular cross-section that retained the similar morphologies of MnOOH nanorods were obtained. The products were characterised by powder X-ray diffraction and field-emission scanning electron microscopy. The influences of different degrees of pH on the morphology and phase of the final products under hydrothermal conditions are discussed. [ABSTRACT FROM AUTHOR]