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Shanxi, China

Zhang T.,Research Institute of Applied BiologyShanxi UniversityTaiyuan | Fan X.,Research Institute of Applied BiologyShanxi UniversityTaiyuan | Song L.,Research Institute of Applied BiologyShanxi UniversityTaiyuan | Ren L.,Research Institute of Applied BiologyShanxi UniversityTaiyuan | And 5 more authors.
IUBMB Life | Year: 2015

Crude brazilin extract from Sappan wood has demonstrated strong anti tumor activity in the mouse model of human bladder carcinoma and clinical trial for intravesical therapy. Purified brazilin was confirmed the most active molecule in inhibition of bladder carcinoma T24 cells. Brazilin decreased proliferation and viability of T24 cells in a dose- and time-dependent manner, with a calculated LC50 of 32 μg/mL. More than 1,000 of genes were found upregulated and down regulated by brazilin treatment in digital gene expression profiling. Gene ontology analysis indicated that stress response, apoptosis, and cell cycle regulatory pathways were highly enriched. Among the regulated genes, c-Fos was the most and specifically upregulated. Overexpression of c-Fos in T24 cells resulted in tumor cell specific changes in cell morphology and viability. Over expression of stress-responsive gene, HSP70, and other highly upregulated genes did not have any effect on cell growth. Brazilin may inhibit T24 cell growth and trigger cell death through a c-Fos-mediated and tumor cell specific signaling pathway. Further studies of its down stream mediators may help to identify better tumor cell type specific drug targets. © 2015 International Union of Biochemistry and Molecular Biology. Source

Shi T.,Shanxi UniversityTaiyuan | Zhao C.,Shanxi UniversityTaiyuan | Li Z.,Shanxi UniversityTaiyuan | Zhang Q.,Central Laboratory Of Taiyuan Central Hospitalno 1 | Jin X.,Shanxi UniversityTaiyuan
Environmental Toxicology | Year: 2015

Bisphenol A (BPA) is a widely used industrial chemical and also an environmental endocrine disruptor (EED), which serves as a monomer in the manufacture of polycarbonate plastics. BPA enters human body mainly through oral intake, and has been reported as being linked to oncogenesis in many tissues. However, the association of BPA intake with gastrointestinal cancer, such as colon cancer, has received less attention. The present study was conducted to investigate the effects of BPA on the migration of normal colon epithelial cells (NCM460 cells) and further elucidate the underlying mechanisms. Our data showed that 1 × 10-8 M (equivalent to environmental concentration) of BPA potently promoted the migration of NCM460 cells. Interestingly, BPA treatment induced an increase of integrin β1 expression, and the functional blocking of integrin β1 abolished the migration-promoting effects of BPA. Moreover, the results showed that it was estrogen receptor β but not estrogen receptor α that was involved in this migration promotion. In addition, cellular exposure of BPA stimulated the expression and activity of MMP-9, a well-known factor of cell migration. Taken together, these results indicate that environmental concentration of BPA exposure promotes cell migration through activating ERβ-mediated integrin β1/MMP-9 pathway, suggesting exposure to BPA in the colon may present a potential cancer risk. © 2014 Wiley Periodicals, Inc. Source

Yao G.,Shanxi UniversityTaiyuan | Yun Y.,Shanxi UniversityTaiyuan | Sang N.,Shanxi UniversityTaiyuan
Environmental Toxicology | Year: 2015

Sulfur dioxide (SO2) is a ubiquitous air pollutant. The previous studies have documented the adverse effects of SO2 on nervous system health, suggesting that acutely SO2 inhalation at high concentration may be associated with neurotoxicity and increase risk of hospitalization and mortality of many brain disorders. However, the remarkable features of air pollution exposure are lifelong duration and at low concentration; and it is rarely reported that whether there are different responses on synapse when rats inhaled same mass of SO2 at low concentration with a longer term. In this study, we evaluated the synaptic plasticity in rat hippocampus after exposure to same mass of SO2 at various concentrations and durations (3.5 and 7 mg/m3, 6 h/day, for 4 weeks; and 14 and 28 mg/m3, 6 h/day, for 1 week). The results showed that the mRNA level of synaptic plasticity marker Arc, glutamate receptors (GRIA1, GRIA2, GRIN1, GRIN2A, and GRIN2B) and the protein expression of memory related kinase p-CaMKp{cyrillic}α were consistently inhibited by SO2 both in 1 week and 4 weeks exposure cases; the protein expression of presynaptic marker synaptophysin, postsynaptic density protein 95 (PSD-95), protein kinase A (PKA), and protein kinase C (PKC) were increased in 1 week exposure case, and decreased in 4 weeks exposure case. Our results indicated that SO2 inhalation caused differential synaptic injury in 1 week and 4 weeks exposure cases, and implied the differential effects might result from different PKA- and/or PKC-mediated signal pathway. © 2014 Wiley Periodicals, Inc. Source

Zhang Y.,Shanxi UniversityTaiyuan | Ji X.,Shanxi UniversityTaiyuan | Ku T.,Shanxi UniversityTaiyuan | Sang N.,Shanxi UniversityTaiyuan
Environmental Toxicology | Year: 2015

SO2, NO2, and PM2.5 are typical air pollutants produced during the combustion of coal. Increasing evidence indicates that air pollution has contributed to the development and progression of heart-related diseases over the past decades. However, little experimental data and few studies of SO2, NO2, and PM2.5 co-exposure in animals exist; therefore, the relevant mechanisms underlying this phenomenon are unclear. An important characteristic of air pollution is that co-exposure persists at a low concentration throughout a lifetime. In the present study, we treated adult mice with SO2, NO2, and PM2.5 at various concentrations (0.5 mg/m3 SO2, 0.2 mg/m3 NO2 6 h/d, with intranasal instillation of 1 mg/kg PM2.5 every other day during these exposures; or 3.5 mg/m3 SO2, 2 mg/m3 NO2 6 h/d, and 10 mg/kg PM2.5 for 28 d). Blood pressure (BP), heart rate (HR), histopathological damage, and inflammatory and endothelial cytokines in the heart were assessed. The results indicate that co-exposure caused endothelial dysfunction by elevating endothelin-1 (ET-1) expression and repressing the endothelial nitric oxide synthase (eNOS) level as well as stimulating the inflammatory response by increasing the levels of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Additionally, these alterations were confirmed by histological staining. Furthermore, we observed decreased BP and increased HR after co-exposure. Our results indicate that co-exposure to SO2, NO2, and PM2.5 may be a major risk factor for cardiac disease and may induce injury to the hearts of mammals and contribute to heart disease. © 2015 Wiley Periodicals, Inc. Source

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