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1.
Biomedical and Environmental Sciences ; (12): 583-589, 2012.
Article in English | WPRIM | ID: wpr-320395

ABSTRACT

<p><b>OBJECTIVE</b>To examine UVB-induced responses in normal human keratinocytes (HaCaT) and epidermoid carcinoma cells (A431) at the cellular and molecular level, and investigated the protective effect of salidroside.</p><p><b>METHODS</b>Cells irradiated by UVB at various dosage and their viability was assessed by MTT assays, cell cycle was analysed by flow cytometry. The expression of NF-κB, BCL-2, and CDK6 after 50 J/m(2) UVB irradiation were detected by RT-PCR and western blotting.</p><p><b>RESULTS</b>Our results confirmed greater tolerance of A341 cells to UVB-induced damage such as cell viability and cell cycle arrest, which was accompanied by differential expression changes in NF-κB, BCL-2, and CDK6. UVB exposure resulted in HaCaT cells undergoing G(1)-S phase arrest. When treated with salidroside, HaCaT survival was significantly enhanced following exposure to UVB, suggesting great therapeutic potential for this compound.</p><p><b>CONCLUSION</b>Taken together, our study suggests that A431 respond differently to UVB than normal HaCaT cells, and supports a role for NF-κB, CDK6, and BCL-2 in UVB-induced cell G(1)-S phase arrest. Furthermore, salidroside can effectively protect HaCaT from UVB irradiation.</p>


Subject(s)
Humans , Antioxidants , Pharmacology , Apoptosis , Radiation Effects , Carcinoma, Squamous Cell , Cell Cycle Checkpoints , Cell Line, Tumor , Cell Survival , Radiation Effects , Gene Expression Regulation, Neoplastic , Glucosides , Pharmacology , Keratinocytes , Radiation Effects , Phenols , Pharmacology , Ultraviolet Rays
2.
Journal of Southern Medical University ; (12): 1405-1406, 2008.
Article in Chinese | WPRIM | ID: wpr-340810

ABSTRACT

<p><b>OBJECTIVE</b>To study the effect of radiation injury on nitric oxide (NO) concentration in mouse peripheral blood and liver.</p><p><b>METHODS</b>NIH mice were subjected to gamma-ray exposure at 9.0 Gy and transferred immediately in room temperature condition. NO concentrations in the liver and peripheral blood were examined before and at different time points after the exposure.</p><p><b>RESULTS</b>Compared to that before exposure, NO concentration in the peripheral blood and liver significantly increased after gamma-ray exposure. NO concentration in the peripheral blood began to increase 3 h after the exposure, but that in the liver increased till 6 h after the exposure.</p><p><b>CONCLUSION</b>Radiation can cause the increase of NO concentration in the peripheral blood and liver, but different tissues may exhibit different response intensities to radiation.</p>


Subject(s)
Animals , Male , Mice , Gamma Rays , Liver , Metabolism , Radiation Effects , Nitric Oxide , Blood , Metabolism , Radiation Injuries, Experimental , Blood , Metabolism , Time Factors
3.
Journal of Southern Medical University ; (12): 394-397, 2006.
Article in Chinese | WPRIM | ID: wpr-255302

ABSTRACT

<p><b>OBJECTIVE</b>To observe the functional changes of dendritic cells (DCs) after infection by recombinant retrovirus carrying human telomerase reverse transcriptase (hTERT) gene fragment.</p><p><b>METHODS</b>Interleukin-12 (IL-12) levels in DC culture supernatant was determined by enzyme-linked immunosorbent assay (ELISA). The abilities of DCs infected with recombinant retrovirus carrying hTERT gene (hTERT-DCs) and non-infected DCs (N-DCs) to stimulate allogeneic lymphocyte proliferation were evaluated with mixed leukocytes reaction (MLR), and the surface markers of DCs including CD80, CD83, CD86 and HLA-DR were detected by flow cytometry. Cytotoxic T lymphocyte (CTL) assay was performed with CytoTox 96 non-radioactive cytoxicity assay.</p><p><b>RESULTS</b>Compared with N-DCs, hTERT-DCs showed no significant changes in IL-12 secretion and capacity to stimulate allogeneic lymphocytes reaction, but had significantly lower CD83 expression. Specific CTLs induced by hTERT-DCs resulted in higher cytotoxicity against telomerase-positive target cells than that against the negative target cells.</p><p><b>CONCLUSION</b>Infection with the recombinant retrovirus carrying hTERT fragment may jeopardize the maturation of DCs, which, however, still retain their capacity to activate and stimulate lymphocyte proliferation and to prime autologous T lymphocytes to generate specific CTL against hTERT.</p>


Subject(s)
Humans , Cells, Cultured , Dendritic Cells , Cell Biology , Allergy and Immunology , Virology , Genetic Vectors , Interleukin-12 , Recombination, Genetic , Retroviridae , Genetics , Metabolism , T-Lymphocytes, Cytotoxic , Allergy and Immunology , Telomerase , Genetics
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