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#28990335   2017/10/09 Save this To Up

Next-Generation Magnetic Nanocomposites: Cytotoxic and Genotoxic Effects of Coated and Uncoated Ferric Cobalt Boron (FeCoB) Nanoparticles In Vitro.

Metal nanoparticles (NPs) have unique physicochemical properties and a widespread application scope depending on their composition and surface characteristics. Potential biomedical applications and the growing diversity of novel nanocomposites highlight the need for toxicological hazard assessment of next-generation magnetic nanomaterials. Our study aimed to evaluate the cytotoxic and genotoxic properties of coated and uncoated ferric cobalt boron (FeCoB) NPs (5-15 nm particle size) in cultured human dermal fibroblasts (NHDFs). Cell proliferation was assessed via ATP bioluminescence kit, DNA breakage and chromosomal damage were measured by alkaline comet assay and micronucleus test. Polyacryl acid-coated FeCoB NPs (PAA-FeCoB NPs) and uncoated FeCoB NPs inhibited cell proliferation at 10 μg ml-1. DNA strand breaks were significantly increased by PAA-coated FeCoB NPs, uncoated FeCoB NPs and l-cysteine-coated FeCoB NPs (Cys-FeCoB NPs), although high concentrations (10 μg ml-1) of coated NPs (Cys- and PAA-FeCoB NPs) showed significantly more DNA breakage when compared to uncoated ones. Uncoated FeCoB NPs and coated NPs (PAA-FeCoB NPs) also induced the formation of micronuclei. Additionally, PAA coated NPs and uncoated FeCoB NPs showed a negative correlation between cell proliferation and DNA strand breaks, suggesting a common pathomechanism, possibly by oxidation-induced DNA damage. We conclude that uncoated FeCoB NPs are cytotoxic and genotoxic at in vitro conditions. Surface coating of FeCoB NPs with Cys and PAA does not prevent but rather aggravates DNA damage. Further safety assessment and a well-considered choice of surface coating are needed prior to application of FeCoB nanocomposites in biomedicine. This article is protected by copyright. All rights reserved.

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#28968949   2017/10/03 Save this To Up

Diazoxide prevents H2O2-induced chondrocyte apoptosis and cartilage degeneration in a rat model of osteoarthritis by reducing endoplasmic reticulum stress.

Osteoarthritis (OA) is a common disease affecting elderly individuals. Its incidence rises sharply with age, and chondrocyte apoptosis plays a vital role in its pathogenesis. Diazoxide opens mitochondrial ATP-sensitive potassium (mitoKATP) channels and exerts multiple pharmacological effects, including reductions in blood pressure and blood sugar levels. It also exerts anti-apoptotic activities, but the cellular and molecular mechanisms by which diazoxide inhibits chondrocyte apoptosis are unknown, as is whether apoptosis is related to endoplasmic reticulum stress (ERS). In the present study, we explored the mechanism underlying the chondroprotective effect of diazoxide on hydrogen peroxide (H2O2)-stimulated chondrocyte apoptosis in rats with surgically induced OA. A cell counting kit-8 (CCK-8) assay showed that the viability of H2O2-stimulated chondrocytes was enhanced in a dose-dependent manner. However, at a concentration ≥400μM, diazoxide had other, negative effects. The protective effect of diazoxide in vitro included inhibition of the ERS response and of mitochondrial dysfunction induced by H2O2 stimulation. These responses were related to activation of the PERK1/2 and ERK1/2 signaling pathways; the prevention of chondrocyte apoptosis; the down-regulation of caspase-3, Bax, ATF-6 and C/EBP-homologous protein (CHOP) expression; and the up-regulation of Bcl-2 and Col II. In vivo, histological and immunohistochemical analyses of caspase-3 and CHOP expression revealed that diazoxide ameliorated cartilage degeneration in a rat model of OA, as revealed by histological and immunohistochemical analyses of caspase-3 and CHOP expression. Diazoxide suppressed H2O2-triggered chondrocyte apoptosis, and ameliorated cartilage degeneration, by inhibiting the development of ERS.

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#28961281   2017/09/29 Save this To Up

Chronic administration of mitochondrion-targeted peptide SS-31 prevents atherosclerotic development in ApoE knockout mice fed Western diet.

Oxidative stress and inflammatory factors are deeply involved in progression of atherosclerosis. Mitochondrion-targeted peptide SS-31, selectively targeting to mitochondrial inner membrane reacting with cardiolipin, has been reported to inhibit ROS generation and mitigate inflammation. The present study was designed to investigate whether SS-31 could suppress the development of atherosclerosis in vivo.

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#28946875   2017/09/26 Save this To Up

Overexpression of lncRNA IGFBP4-1 reprograms energy metabolism to promote lung cancer progression.

Reprogrammed energy metabolism as an emerging hallmark of cancer has recently drawn special attention since it facilitate cell growth and proliferation. Recently, long noncoding RNAs (lncRNAs) have been served as key regulators implicated in tumor development and progression by promoting proliferation, invasion and metastasis. However, the associations of lncRNAs with cellular energy metabolism in lung cancer (LC) need to be clarified.

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#28912867   2017/09/15 Save this To Up

Protective effect of controlled release of cytokine response modifier A from chitosan microspheres on rat chondrocytes from interleukin-1β induced inflammation and apoptosis.

The aim of the present study was to investigate the protective effect of cytokine response modifier A (CrmA) released from chitosan (CS) microspheres in a controlled manner on interleukin (IL)-1β-induced inflammation and apoptosis in chondrocytes. The CrmA release kinetics were characterized by an initial burst release, which was reduced to a linear release over 8 days. Furthermore, chondrocytes were isolated from 1-week-old Sprague Dawley rats. The cell culture was established by stimulation with 10 ng/ml IL-1β and subsequent incubation with CS-CrmA microspheres. Following stimulation with IL-1β, the viability of chondrocytes was decreased. However, the cell viability was attenuated by CS-CrmA microspheres as revealed by a cell counting kit-8 assay. CS-CrmA microspheres significantly inhibited IL-1β-induced inflammation in chondrocytes by attenuating increases in the gene expression levels of inducible nitric oxide synthase and cyclooxygenase-2, as well as the concentrations of nitric oxide and prostaglandin E2. CS-CrmA microspheres significantly decreased the number of apoptotic chondrocytes induced by IL-1β as indicated by a terminal deoxyribonucleotide transferase deoxyuridine triphosphate nick-end labeling assay. In addition, CS-CrmA microspheres blocked IL-1β-induced chondrocyte apoptosis by increasing B-cell lymphoma 2 (Bcl-2) and decreasing Bcl-2-associated X protein, caspase-3 and poly adenosine diphosphate-ribose polymerase expression at the mRNA and protein levels, as indicated by reverse-transcription quantitative polymerase chain reaction and western blot analysis, respectively. The results of the present study revealed that CS-CrmA microspheres, as a controlled release system of CrmA, may protect rat chondrocytes from IL-1β-induced inflammation and apoptosis via regulating inflammatory and apoptosis-associated genes.

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#28852730   2017/08/30 Save this To Up

DIFFERENT CONCENTRATIONS OF SIJUNZI DECOCTION INHIBIT PROLIFERATION AND INDUCE APOPTOSIS OF HUMAN GASTRIC CANCER SGC-7901 SIDE POPULATION.

Sijunzi Decoction (SD) is a traditional Chinese medicine which is composed of Ginseng, Atractylodes, Poria and Licorice. It is one of the commonly used Chinese traditional medicines that showed anti-gastric cancer activity in clinical studies. Previous evidence demonstrated SD parties (Ginseng, Atractylodes, Poria, Licorice) can inhibit proliferation and induced apoptosis for gastric cancer cell. In order to further investigate the anticancer effect of SD in gastric cancer, we observed the effects of different concentrations of SD on proliferation and apoptosis of Side Population Cells (SP) of human gastric cancer SGC-7901.

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#28814962   2017/08/17 Save this To Up

Circulating zinc-α2-glycoprotein levels are low in newly diagnosed patients with metabolic syndrome and correlate with adiponectin.

Zinc-α2-glycoprotein (ZAG) is a novel adipokine that reduces insulin resistance, protecting against type 2 diabetes. However, past studies have been contradictory. This cross-sectional study aims to investigate the association of circulating ZAG with metabolic syndrome (MetS) in middle-aged and older Chinese adults.

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#28793908   2017/08/10 Save this To Up

Transcriptomic analysis comparing mouse strains with extreme total lung capacities identifies novel candidate genes for pulmonary function.

Failure to attain peak lung function by early adulthood is a risk factor for chronic lung diseases. Previously, we reported that C3H/HeJ mice have about twice total lung capacity (TLC) compared to JF1/MsJ mice. We identified seven lung function quantitative trait loci (QTL: Lfnq1-Lfnq7) in backcross/intercross mice derived from these inbred strains. We further demonstrated, superoxide dismutase 3, extracellular (Sod3), Kit oncogene (Kit) and secreted phosphoprotein 1 (Spp1) located on these Lfnqs as lung function determinants. Emanating from the concept of early origin of lung disease, we sought to identify novel candidate genes for pulmonary function by investigating lung transcriptome in C3H/HeJ and JF1/MsJ mice at the completion of embryonic development, bulk alveolar formation and maturity.

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#28785292   2017/08/08 Save this To Up

Dahuang Zhechong Pill Combined with Doxorubicin Induces Cell Death through Regulating Energy Metabolism in Human Hepatocellular Carcinoma Cells.

Many physiological activities such as cell survival, proliferation, defense, adaptation, and metabolism need to consume energy. Hepatoma cells can quickly start stress responses like multidrug resistance (MDR) requiring adenosine triphosphate (ATP) consumption after administration of chemotherapeutics. We employed CCK-8 assay to evaluate cell viability and the flow cytometry to confirm apoptosis and necrosis. ELISA kit was used to determine intracellular levels of ATP in lysates. Western blot was employed to analyze the expressions of key enzymes involved in energy metabolism. We found that doxorubicin (DOX) potently stimulated apoptosis at a low dose and even induced necrosis at a high dose in SMMC-7721. DHZCP combined with DOX at low or middle dose enhanced the synergistic antihepatoma effect. Results indicated that Dahuang Zhechong Pill (DHZCP) inhibited the expressions of several key enzymes involved in oxidative phosphorylation and reduced intracellular ATP levels. The combination of DHZCP with DOX reversed the elevation of intracellular ATP levels, and a significantly synergistic antitumor effect was observed. DHZCP could not only strengthen the therapeutic effects of chemotherapeutic drugs but also decrease the doses of chemotherapeutic drugs and the incidences of adverse reactions, providing novel strategies for clinical treatment of liver cancer.

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#28782285   2017/08/07 Save this To Up

Metformin enhances doxorubicin sensitivity via inhibition of doxorubicin efflux in P-gp-overexpressing MCF-7 cells.

Resistance against chemotherapy is still a major problem in successful cancer treatment in the clinic. Therefore, identifying new compounds with lower side-effects and higher efficacy is an important approach to overcome multidrug resistance (MDR). Here, we investigated the activity and possible mechanism of the antidiabetic drug, metformin, in human doxorubicin (DOX)-resistant breast cancer (MCF-7/DOX) cells. The effect of metformin on the cytotoxicity of DOX was evaluated by MTT assay. The P-gp mRNA/protein expression levels following treatment with metformin were determined using real-time polymerase chain reaction and Western blot analysis, respectively. Intracellular rhodamine 123 accumulation assay was performed to evaluate the P-gp function. Cellular ATP content was determined using ATP assay kit. The effect of metformin on DOX-induced apoptosis was evaluated by annexin V/FITC assay. Exposure to metformin considerably enhanced the cytotoxicity of DOX. Metformin had no substantial effect on P-gp expression, while the activity of P-gp and intracellular ATP content decreased with metformin treatment in a dose-dependent manner. Furthermore, metformin significantly increased the DOX-induced apoptosis. These results indicate that metformin could reverse MDR in breast cancer cells by reducing P-gp activity. Therefore, metformin can be suggested as a potent adjuvant in breast cancer chemotherapy.

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