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Li Y.,Central China Normal University | Tian X.,Wuhan University | Lu Z.,Nanyang Technological University | Yang C.,Wuhan University | And 6 more authors.
Journal of Nanoscience and Nanotechnology | Year: 2010

α-Manganese dioxide (α-MnO 2) nanowires are used as electrode materials to significantly enhance the performance of lithium batteries. In this study, we investigate the nanotoxicity of α-MnO 2 nanowires toward Hela cells. The α-MnO 2 nanowires, which were successfully synthesized using the hydrothermal approach, can induce cytotoxicity dose-dependently in Hela cells. The accumulation of reactive oxygen species (ROS) and depletion of glutathione (GSH) are also observed in the nanowire-treated cells. In addition, comet assays and cell nucleus morphology show that both DNA damage and cell apoptosis occur in the nanowires exposure group. Based on these results, a mechanism for α-MnO 2 nanowire-induced cytotoxicity in Hela cells, which involves the accumulation of ROS, formation of oxidative stress, DNA oxidative damage and cell apoptosis, is proposed. This investigation may provide a fundamental insight to understand the nanotoxicity of wire-shaped nanomaterials. Copyright © 2010 American Scientific Publishers All. rights reserved. Source


Tang Y.,Beijing Institute of Pharmacology and Toxicology | Tang Y.,Chongqing Medical University | Long C.-L.,Beijing Institute of Pharmacology and Toxicology | Wang R.-H.,Thadweik Academy of Medicine | And 4 more authors.
Journal of Cardiovascular Pharmacology | Year: 2010

We sought to explore new strategies targeting SUR2B/Kir6.1, a subtype of adenosine triphosphate (ATP)-sensitive potassium channels (KATP), against pressure overload-induced heart failure. The effects of natakalim, a SUR2B/Kir6.1 selective channel opener, on progression of cardiac remodeling were investigated. Pressure overload-induced heart failure was induced in Wistar rats by abdominal aortic banding. The effects of natakalim (1, 3, and 9 mg·kg-1·d-1 for 10 weeks) on myocardial hypertrophy and heart failure, cardiac histology, vasoactive compounds, and gene expression were assessed. Ten weeks after the onset of pressure overload, natakalim treatment potently inhibited cardiac hypertrophy and prevented heart failure. Natakalim remarkably inhibited the changes of left ventricular hemodynamic parameters and reversed the increase of heart mass index, left ventricular weight index, and lung weight index. Histological examination demonstrated that there was no significant hypertrophy or fibrosis in pressure-overloaded hearts of natakalim-treated rats. Ultrastructural examination of hearts revealed well-organized myofibrils with mitochondria grouped along the periphery of longitudinally oriented fibers in rats from the natakalim group. The content of serum nitric oxide and plasma prostacyclin was increased, whereas that of plasma endothelin-1 and cardiac tissue hydroxyproline and atrial and B-type natriuretic peptide messenger RNA was downregulated in natakalim-treated rats. Natakalim at 0.01-100 μM had no effects on isolated working hearts derived from Wistar rats; however, natakalim had endothelium-dependent vasodilatory effects on the isolated tail artery helical strips precontracted with norepinephrine. These results indicate that natakalim reduces heart failure caused by pressure overloading by activating the SUR2B/Kir6.1 KATP channel subtype and protecting against endothelial dysfunction. Copyright © 2010 by Lippincott Williams & Wilkins. Source


Ma P.,University of Science and Technology of China | Ma P.,Central China Normal University | Luo Q.,Central China Normal University | Chen J.,University of Science and Technology of China | And 5 more authors.
International Journal of Nanomedicine | Year: 2012

Because of its unique magnetic properties, the iron oxide (Fe3O4) nanoparticle has been widely exploited and its application in various fields has promised immense benefits. However, doubts exist over the use of Fe3O4-nanoparticles in human beings. Thus, the aim of the current study was to find out the potential safety range of medical use. Twenty-five Kunming mice were exposed to Fe3O4-nanoparticles via intraperitoneal injection daily for 1 week at doses of 0, 5, 10, 20, and 40 mg/kg. Hepatic and renal tissues were sliced for physiological observation. Injuries were observed in the high-dose groups (20 and 40 mg/kg) compared with the control group (0 mg/kg). Biomarkers of reactive oxygen species, glutathione, malondialdehyde, DNA-protein crosslinks, and 8-hydroxy-2′-deoxyguanosine in the hepatic and renal tissues were detected. Injury to tissues and oxidative damage to cells at the molecular level was found. The safest dose recommended from the results of this study is 5 mg/kg, as we believe this to be an upper limit balancing the benefits and risks for sub-long-term exposure. © 2012 Ma et al, publisher and licensee Dove Medical Press Ltd. Source


Ren Z.,Tianjin Institute of Health and Environmental Medicine | Ren Z.,Chinese Institute of Basic Medical Sciences | Gu X.,Xuzhou Medical College | Gu X.,China Pharmaceutical University | And 9 more authors.
Journal of Cellular and Molecular Medicine | Year: 2016

The development of multidrug resistance (MDR) not only actively transports a wide range of cytotoxic drugs across drug transporters but is also a complex interaction between a number of important cellular signalling pathways. Nitric oxide donors appear to be a new class of anticancer therapeutics for satisfying all the above conditions. Previously, we reported furoxan-based nitric oxide-releasing compounds that exhibited selective antitumour activity in vitro and in vivo. Herein, we demonstrate that bifendate (DDB)-nitric oxide, a synthetic furoxan-based nitric oxide-releasing derivative of bifendate, effectively inhibits the both sensitive and MDR tumour cell viability at a comparatively low concentration. Interestingly, the potency of DDB-nitric oxide is the independent of inhibition of the functions and expressions of three major ABC transporters. The mechanism of DDB-nitric oxide appears to be in two modes of actions by inducing mitochondrial tyrosine nitration and apoptosis, as well as by down-regulating HIF-1α expression and protein kinase B (AKT), extracellular signal-regulated kinases (ERK), nuclear factor κB (NF-κB) activation in MDR cells. Moreover, the addition of a typical nitric oxide scavenger significantly attenuated all the effects of DDB-nitric oxide, indicating that the cytotoxicity of DDB-nitric oxide is as a result of higher levels of nitric oxide release in MDR cancer cells. Given that acquired MDR to nitric oxide donors is reportedly difficult to achieve and genetically unstable, compound like DDB-nitric oxide may be a new type of therapeutic agent for the treatment of MDR tumours. © 2016 John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. Source


Gu X.,Xuzhou Medical College | Gu X.,China Pharmaceutical University | Tang X.,China Pharmaceutical University | Zhao Q.,Tianjin Institute of Health and Environmental Medicine | And 3 more authors.
Bioorganic and Medicinal Chemistry Letters | Year: 2014

We recently reported alkoxyl biphenyl derivatives bearing dibenzo[c,e]azepine scaffold as novel P-glycoprotein (P-gp, ABCB1) inhibitors. In this study, their ability to reverse breast cancer resistance protein (BCRP, ABCG2)-mediated multidrug resistance was tested in HEK293/BCRP cells which was BCRP-transfected stable HEK293 cells. It was observed that compounds 4d, 4h, 4i increased mitoxantrone accumulation in HEK293/BCRP cells via inhibiting BCRP efflux function. Notably, the inhibitory activity of 4i was comparable to that of the classical BCRP inhibitor Ko143 at an equimolar concentration. Interestingly, 4i had little inhibitory effect on multidrug resistance- associated protein 1 (MRP1, ABCC1), another drug efflux transporter. These results, together with the previous findings, suggest that 4i may be a dual inhibitor of P-gp and BCRP to warrant further investigation. © 2014 Elsevier Ltd. All rights reserved. Source

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