Yanhui Zhou

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This paper reported the preparation and antioxidant capacities of element selenium nanoparticles (nanoSe(0))-ascorbic acid (Vc) sol and nanSe(0)/Vc/selenocystine (SeCys) sol-gel compounds. NanoSe(0)-Vc sol was prepared by reduction of selenious dioxide (SeO2) with Vc. In the nanoSe(0)-Vc sol, highly concentrated Vc was also used as a modifier to modulate(More)
The interaction of ruthenium (II) complex [Ru(bpy)2(mal)]2+ (RBM) and [Ru(phen)2(mal)]2+ (RPM) (bpy = 2, 2-bipyridine, phen = 1,10-phenanthroline, mal = malonyl carboxylate) with human serum albumin (HSA) has been investigated by using fluorescence, UV absorption and circular dichroism (CD) spectroscopy approaches. A strong fluorescence quenching reaction(More)
Amyloid-beta (Aβ) has a pivotal function in the pathogenesis of Alzheimer's disease. To investigate Aβ neurotoxicity, we used an in vitro model that involves Aβ25-35-induced cell death in the nerve growth factor-induced differentiation of PC12 cells. Aβ25-35 (20μM) treatment for 24h caused apoptotic cell death, as evidenced by significant cell viability(More)
Anti-angiogenesis is an effective strategy for cancer treatment because uncontrolled tumor growth depends on tumor angiogenesis and sufficient blood supply. Thus, blocking angiogenesis could be a strategy to arrest tumor growth. The function and mechanism of luminescent ruthenium-modified selenium nanoparticles (Ru-SeNPs) in angiogenesis have not been(More)
Metal ions promote Alzheimer's disease (AD) pathogenesis by accelerating amyloid-β (Aβ) aggregation and inducing formation of neurotoxic reactive oxygen species (ROS) such as hydrogen peroxide (H2O2). Although metal chelators can block these effects, their therapeutic potential is marred by their inability to cross the blood-brain barrier (BBB) and by their(More)
Here we reported the high tumor targeting efficacy of luminescent Ru(II)-thiols protected selenium nanoparticles (Ru-MUA@Se). We have shown that a dual-target inhibitor Ru-MUA@Se directly suppress the tumor growth but also block blood-vessel growth. We also determined that the nanoparticles entered the cells via clathrin-mediated endocytosis pathway. In a(More)
Alzheimer's disease (AD), the most common neurodegenerative disease, is caused by an accumulation of amyloid-β (Aβ) plaque deposits in the brains. Evidence is increasingly showing that epigallocatechin-3-gallate (EGCG) can partly protect cells from Aβ-mediated neurotoxicity by inhibiting Aβ aggregation. In order to better understand the process of Aβ(More)
Functionalization can promote the uptake of nanoparticles into cancer cells via receptor-mediated endocytosis, enabling them to exert their therapeutic effects. In this paper, epigallocatechin gallate (EGCG), which has a high binding affinity to 67 kDa laminin receptor (67LR) overexpressed in HCC cells, was employed in the present study to functionalized(More)
Two arene ruthenium complexes [Ru(η(6)-C(6)H(6))(p-MOPIP)Cl](+)1 and [Ru(η(6)-C(6)H(6))(p-CFPIP)Cl](+)2, where p-MOPIP = 2-(4-methoxyphenyl)-imidazo[4,5f][1,10] phenanthroline and p-CFPIP = 2-(4-trifluoromethylphenyl)-imidazo[4,5f][1,10] phenanthroline, were prepared and the interactions of these compounds with DNA oligomers 5'-G3(T2AG3)3-3'(HTG21) have(More)
In the present study, the interaction between GC-rich sequence of bcl-2 gene P1 promoter (Pu39) and two ruthenium (II) polypyridyl complexes, [Ru(bpy)2(tip)]2+ (1) and [Ru(phen)2(tip)]2+ (2), was investigated by UV–Visible, fluorescence spectroscopy, circular dichroism, fluorescence resonance energy transfer melting assay and polymerase chain reaction stop(More)