Ying Wang

Capital Medical University, Peping, Beijing, China

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Publications (3)2.91 Total impact

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    ABSTRACT: The purpose of this research was to investigate the effects of testosterone propionate on oxidative stress and cytokine gene expression in endosulfan-treated mice. The levels of endosulfan and testosterone propionate were 0 and 0 mg x kg-1 x d(-1) (control group), 0.8 and 0 mg x kg-1 x d(-1) (endosulfan-treated group), and 0.8 and 10 mg x kg(-1) x d(-1) (experimental group), respectively. The results showed that total antioxidation capability (T-AOC) in the endosulfan-treated group was reduced significantly when compared with the control group, whereas the levels of malondialdehyde (MDA) and hydroxyl free radicals increased when compared with the control group. T-AOC levels in the experimental group were higher than that of the endosulfan-treated group, and the levels of MDA and hydroxyl free radicals decreased when compared with the endosulfan-treated group. The messenger RNA (mRNA) levels of interleukin (IL)-2 and IL-6 in the endosulfan-treated group were significantly higher than that of the control group. The mRNA levels of IL-6 in the experimental group were lower than that of the endosulfan-treated group, whereas the mRNA levels of IL-2 and interferon-γ had no significant difference between the 2 groups. The results suggest that testosterone propionate alleviates oxidative stress induced by endosulfan and at least partially reverses the changes of cytokine gene expression in mice. It is possible that androgens affect cytokine expression by alleviating oxidative stress induced by endosulfan.
    Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer. 01/2012; 31(1):17-26.
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    ABSTRACT: The purpose of this study was to investigate the effects of vitamin E on reproductive hormones and testis structure in mice treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Five experimental groups of a combination of TCDD and vitamin E were designed as follows: 0 ng/kg/d and 0 mg/kg/d (control group), 100 ng/kg/d and 0 mg/kg/d (Group I), 100 ng/kg/d and 20 mg/kg/d (Group II), 100 ng/kg/d and 100 mg/kg/d (Group III), and 100 ng/kg/d and 500 mg/kg/d (Group IV) respectively. Vitamin E and TCDD were given by oral gavage for 7 weeks. The results demonstrated that TCDD decreased the levels of brain gonadotropin releasing hormone (GnRH), testis luteinizing hormone (LH) and follicle stimulating hormone (FSH), serum testosterone and testis spermatozoa number, and damaged testis structure. Vitamin E at 20 mg/kg alleviated the decrease of GnRH; vitamin E at 20, 100, and 500 mg/kg antagonized the decline of LH and FSH; vitamin E at 20 and 100 mg/kg reversed the decrease of testosterone and spermatozoa number; and vitamin E at 100 mg/kg decreased the damage of the testis structure caused by TCDD. The results indicate that vitamin E antagonizes the reproductive endocrine toxicity and alleviates the changes in testicular structure caused by TCDD.
    Toxicology and Industrial Health 06/2011; 28(2):152-61. · 1.56 Impact Factor
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    ABSTRACT: The study was conducted to investigate the effects of vitamin E on NK cell activity and lymphocyte proliferation in tr eated female mice by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In chronic TCDD trial, 45 mice were divided into 5 groups, and the levels of TCDD and vitamin E were 0 and 0, 100 and 0, 100 and 20, 100 and 100, and 100 ng/kg/d and 500 mg/kg/d, respectively. In acute TCDD trial, 24 mice were divided into three groups, and the levels of TCDD and vitamin E were 0 and 0, 30 and 0, and 30 microg/kg and 100 mg/kg, respectively. The results showed chronic TCDD-treatment caused decrease tendencies of spleen NK cell activity and lymphocyte proliferation, and vitamin E 100mg/kg alleviated the decreases tendencies caused by chronic TCDD-treatment, and the lymphocyte proliferation in the group given vitamin E 100mg/kg was significantly higher than that of the chronic TCDD-treated group. Acute TCDD-treatment suppressed the NK cell activity and lymphocyte proliferation, and vitamin E 100mg/kg significantly alleviated the decrease caused by acute TCDD-treatment. These results suggested that TCDD resulted in immunotoxicity, and the toxicity of acute TCDD-treatment was severe compared with chronic TCDD, while vitamin E alleviated the immunotoxicity from TCDD.
    Immunopharmacology and Immunotoxicology 04/2009; 31(3):432-8. · 1.36 Impact Factor

Publication Stats

4 Citations
2.91 Total Impact Points

Institutions

  • 2011–2012
    • Capital Medical University
      • • School of Public Health and Family Medicine
      • • School of Basic Medical Sciences
      Peping, Beijing, China