[Mechanism of Triclosan in the Treatment of Nonalcoholic Fatty Liver Disease Based on Network Pharmacology].

Objective To explore the potential targets of triclosan in the treatment of nonalcoholic fatty liver disease(NAFLD) and to provide new clues for the future research on the application of triclosan. Methods The targets of triclosan and NAFLD were obtained via network pharmacology.The protein-protein interaction network was constructed with the common targets shared by triclosan and NAFLD.

[Comparative Analysis of Direct Drinking Water and the Relevant Sanitation Standards in China].

Along with the economic and technological development and growing demand for high-quality drinking water, direct drinking water has gained general popularity in China. However, no authoritative policy has been issued, giving a clear definition of direct drinking water and existing standards and regulations concerning direct drinking water are not definitive in nature. Existing water quality parameters are not well supported and sometimes even contradict each other.

Preoperative serum ferritin is an independent prognostic factor for liver cancer after hepatectomy.

Background And Aims: Serum ferritin (SF) may have a close relationship with the tumor. But no study has investigated the prognostic value of SF in hepatocellular carcinoma (HCC) patients receiving curative resection yet. Aim of this study is to explore the role of preoperative SF in survival outcomes of such patients.

[miR-155/BACH1 Signaling Pathway in Human Lung Adenocarcinoma Cell Death Induced by Arsenic Trioxide].

Objective: To explore the changes of micro RNA 155 (miR-155),BTB and CNC homologous protein 1 (BACH1),quinone oxidoreductase 1 (NQO1) and heme-oxygenase-1 (HO-1) in the process of arsenic trioxide-induced cell death,and to clarify the relationship between miR-155 and BACH1,providing experimental basis for the sensitivity of arsenic trioxide (ATO) treatment.

Methods: Human lung adenocarcinoma cell line A549 cells were treated with different concentrations of ATO. MTT assay and total antioxidant capacity detection kit were used to determine cell viability and total antioxidant capacity,respectively.

[Effect of Cell Autophagy on the Apoptosis of Hepatocellular Carcinoma Cells Induced by Arsenic Trioxide].

Objectives: To determine the effect of autophagy on the apoptosis of hepatocellular carcinoma cells induced by arsenic trioxide (ATO).

Methods: Hepatocellular carcinoma HepG2 cells were exposed to ATO. The cell viability was detected by MTT after adjustments for autophagy agonist (Rap) and autophagy inhibitor (3-MA).

[The Protective Effect of Inhibition of PARP-1 on Inflammation Induced by PM2.5 in Human Bronchial Epithelial Cell Line.].

Objectives: To explore whether the inhibition of poly ADP-ribose polymerase-1(PARP-1) could attenuated inflammation induced by fine particulate matter (PM2.5) in human bronchial epithelial cell line.

Methods: Cell viability was detected by Trypan Blue assay after incubated with PM2.

[The Experiment Study and Mechanism of Aspirin Enhances Cellular Sensitivity of Hepatocellular Carcinoma Cell Line to Arsenic Trioxide].

Objective: To explore whether aspirin could sensitize arsenic trioxide on human hepatocelluar carcinoma cell line and understanding the combination mechanisms underlying co-treatment.

Methods: Cell viability was detected by MTT assay, cell apoptosis rate and reactive oxygen species (ROS) level were measured by flow cytometry, and Western blot assay was used to estimated the protein expression of heme oxygenase-1 (HO-1) in total protein and NF-E2-related factor 2 (Nrf2) in nuclear protein.

Results: 10 μmol/L arsenic trioxide can decreased the cell viability, while cell apoptosis rate, ROS level, HO-1 and Nrf2 protein expression was increased (P < 0.

[4-amino-1,8-naphthalimide on the Sensitive effect of arsenic trioxide in hepatocellular carcinoma cells].

Objective: To study the effect and mechanism of 4-amino-1, 8-naphthalimide (4-AN) on the sensitive effect of arsenic trioxide (ATO) in hepatocellular carcinoma cells.

Methods: Hepatocellular carcinoma HepG2 cells were divided into two groups according to whether they were treated with 4-AN or not. Cell viability was evaluated by MTT assay, population doubling experiment and colony formation assay; genic mechanism was explored by 8-OH-dG assay, single cell gel electrophoresis (comet assay) and microriucleus test.

Critical role of cellular glutathione homeostasis for trivalent inorganic arsenite-induced oxidative damage in human bronchial epithelial cells.

Trivalent inorganic arsenic (iAs(3+)) is a powerful carcinogen that enhances the risk of lung cancer. Paradoxically, iAs(3+) also shows substantial efficacy in the treatment of lung tumors. However, the exact molecular mechanisms underlying iAs(3+)-induced toxicity and therapeutic effect in lung remain unclear.

[The apoptotic mechanism of hepatocellular carcinoma cell line (HepG2) induced by arsenic trioxide].

Objective: To explore the apoptotic mechanism of human hepatic carcinoma cell line HepG2 induced by arsenic trioxide (As2O3).

Methods: The human hepatoma cell line HepG2 was treated with 0, 2.5, 5 and 10 micromol/L arsenic trioxide for 24 h.

The protective role of resveratrol in the sodium arsenite-induced oxidative damage via modulation of intracellular GSH homeostasis.

Sodium arsenite (NaAsO2) is a well-established environmental carcinogen that has been found to cause various human malignant tumors. Thus, how to prevent the deleterious effects caused by NaAsO2 has received widely concerns. Resveratrol (3,4',5-trihydroxystilbene), a polyphenol found in numerous plant species, has recently been known as a natural and powerful antioxidant.

[Construction and expression of the eukaryotic expression vector containing AIF gene].

Objective: To construct the eukaryotic express vector containing apoptosis-inducing factor (AIF) gene and to study its expression in A549 cells.

Methods: According to the GenBank AIF mRNA sequence, specific primers to amplify AIF gene from lung carcinoma cell line A549 by RT-PCR was designed. The amplified AIF gene fragment was cloned into plasmid pUC-T by TA cloning, then double enzyme digestion and DNA sequencing were used to identifying the positive recombinant AIF-pUC-T.

Dual role of resveratrol in modulation of genotoxicity induced by sodium arsenite via oxidative stress and apoptosis.

The potential benefits of resveratrol as an anticancer (proapoptosis) and antioxidant (pro-survival) compound have been studied extensively. However, the role of resveratrol in modulation of the toxicity induced by sodium arsenite (NaAsO₂) is still unclear. In the present study, we examined the effects of resveratrol on NaAsO₂-induced cytotoxicity, DNA and chromosomal damage, cell cycle progression, apoptosis and oxidative stress in human lung adenocarcinoma epithelial (A549) cell line at concentrations from 1 to 20 μM after 24h exposure.

[Mechanism of DNA polymerase beta hyper-expression in malignant transformation induced by benzo[a] pyrene].

Objective: To explore the mechanism of the hyper-expression of DNA polymerase beta (polbeta) in benzo[a]pyrene (BaP) induced malignant transformed cell (polbeta-T).

Methods: The mutation of polbeta gene exon and promoter were examined using reverse transcriptase-polymerase chain reaction-single strand conformation polymorphism (RT-PCR-SSCP) and gene sequencing. The expression of protein-arginine N-methyhransferase 6 (PRMT6) mRNA and protein in polbeta-T cell and control cell (polbeta cell) were investigated by RT-PCR and Western blot.

[Effect of DNA polymerase beta on apoptosis and mitochondrial membrane potential induced by hydroquinone, a metabolite of benzene].

Objective: To explore the effect and mechanism of DNA polymerase β expression level on cell apoptosis and mitochondrial membrane potential induced by hydroquinone.

Methods: Polβ wild-type cells (polβ+/+), polβ overexpressed cells (polβ oe) and polβ null cells (polβ-/-) were applied as a model cell system, The effect of cell apoptosis and mitochondrial membrane potential induced by different doses of hydroquinone were analyzed by flow cytometry. The ROS and ·OH assay kit were used to examine the cellular ROS and ·OH level.

[Effects of DNA polymerase beta on the genotoxicity and genetic instability induced by benzo(a)pyrene].

Objective: To explore the effects of DNA polymerase β expression level on the genotoxicity and genetic instability induced by benzo(a)pyrene (BaP),and provide experimental the basis for further study on the carcinogenic molecular mechanism of BaP.

Methods: Three kinds of cell lines with the identical genetic background, polβ wild-type cells (polβ+/+), polβ null cells (polβ-/-) and polβ overexpression cells (polβ oe) were applied as cellular models. The oxidative damage, genotoxicity and genetic instability induced by BaP were analyzed by using different methods respectively.

[Exploration of relationship between the expression level of DNA polymerase beta and 60Co gamma-ray radiosensitivity].

Objective: To explore the relationship between the expression level of DNA polymerase beta (pol beta) and 60Co gamma-ray radiosensitivity and provide a basis on improving the efficiency of radiotherapy theoretically.

Methods: pol beta wild-type cells (pol beta +/+), pol beta null cells (pol beta -/-) and pol beta overexpressed cells (polp beta oe) were applied as a model system. The radiosensitivity of 60Co gamma-ray on the cell was detected by MTT assay and clone formation assay.

[Effects of pol beta on biological characteristics and DNA damage in mouse embryonic fibroblast].

Objective: To explore the effect of DNA polymerase beta (pol beta) expression level on biological characteristics of mouse embryonic fibroblast (MEF) and the cellular response to DNA damage induced by potassium dichromate.

Methods: pol beta wild-type cells (pol beta +/+), pol beta null cells (pol beta -/-) and pol beta overexpressed cells (pol beta oe) were applied as a model system. The growth curve of cells was plotted by MTT assay; the doubling time of cells was detected by double time experiment; the spontaneous mutation frequency was determined by HGPRT gene mutation method and single cell gel electrophoresis assay (SCGE) was employed to observe the DNA damage either happened spontaneously or induced by potassium dichromate.

[Effect of down-regulated hOGG1 gene expression on cytotoxicity and genotoxicity of hydroquinone].

Objective: To explore the effects of down- regulated hOGG1 gene expression on cytotoxicity and genotoxicity of hydroquinone.

Methods: A549 cells and A549-R cells with down- regulated hOGG1 gene were treated with different concentrations of hydroquinone (0, 5, 10, 20, 40 and 80 μmol/L). The cellular sensitivity and contents of ROS were measured by MTT assay and fluorescence method, respectively.

[Effect of metabolism activation on the oxidative cell damage induced by cigarette smoking].

Objective: To explore the effect of metabolic activation on the oxidative cell damage induced by mainstream smoke (MS).

Methods: A549 cells were treated with different concentrations of MS for 2 hours in the presence and absence of S9 mix. ROS levels were determined.

[Cigarette smoke-induced oxidative damage to human bronchial epithelial cells].

Objective: To determine the oxidative damage of mainstream smoke (MS) on Human bronchial epithelial cells (HBE) and its role in lung cancer.

Methods: MTT assay was used to test the cytotoxicity of MS on HBE. The HBE cells were treated with different concentrations of MS for 12 h.

[Effects of hydroquinone on expression of human 8-oxo-guanine DNA glycosylase mRNA in human A549 lung adenocarcinoma cell strains].

Objective: To explore the effects of hydroquinone (HQ) on reactive oxygen species (ROS) generation, antioxydase activities and the expression of human 8-oxo-guanine DNA glycosylase (hOGG1) mRNA in human A549 lung adenocarcinoma cell strains.

Methods: A549 cells were treated with different concentrations of HQ. Cell survival was determined by methyl thiazolyl tetrazolium (MTT).

[Oxidative damage of gasoline engine exhausts to rat lung tissues].

Objective: To study the effects of extracts of condensate, particulates and semivolatile organic compounds from gasoline engine exhaust on DNA damage, 8-oxoguanine DNA glycosylase-1 (OGG1) expression, and changes of ultra-structures in lungs of rats.

Methods: Organic extracts of gasoline engine exhaust (GEE) was intratrachealy instilled into rat lungs at 0, 5.6, 16.

[Molecular epidemiological study on oxidative DNA damage among Hasake ethnic migrants in Shenzhen].

Objective: To explore the relationship of migration and oxidative DNA damage by comparative study of oxidative DNA damage effects on people with different years of migration among Xinjiang Hasake ethnicity in Shenzhen.

Methods: Sixty Hasake residents in Shenzhen were selected, and were divided into three groups (n=20) according to the years of migration. Major changes of their life style were investigated.

[Effects and mechanism of lutein on apoptosis of esophageal carcinoma EC9706 cells].

Objective: To study the effects of lutein on apoptosis and its mechanism.

Method: The cells of human esophageal carcinoma EC9706 were grown in RPMI medium containing 10% bovine serum and were treated with lutein at 100 microg x mL(-1) concentration. Flow cytometry was employed to investigate the effects of lutein on cell apoptosis of EC9706 cells.