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The Intervention Effect of Rosiglitozone in Ovarian Fibrosis of PCOS Rats

Objective To explore the Intervention effect of Rosiglitozone in ovarian fibrosis of PCOS rats. Methods 60 female SD rats were randomly divided into 3 groups: control group, model group and treatment group. The model and treatment groups were established by subcutaneous injection of DHEA, while the...

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Published in:Biomedical and environmental sciences 2012-02, Vol.25 (1), p.46-52
Main Authors: MIAO, Zhu Lin, GUO, Liang, WANG, Yong Xia, CUI, Rong, YANG, Ning, HUANG, Mi Qiong, QIN, Wei Bing, CHEN, Jin, LI, Hong Mei, WANG, Zi Neng, WEI, Xiang Cai
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Language:English
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Summary:Objective To explore the Intervention effect of Rosiglitozone in ovarian fibrosis of PCOS rats. Methods 60 female SD rats were randomly divided into 3 groups: control group, model group and treatment group. The model and treatment groups were established by subcutaneous injection of DHEA, while the treatment group was given RGZ. The serum hormone values, pathohistology of ovarian structure of rats, ovarian ultrastructure and the expressions of TGF-β1 and CTGF were detected. Results The PCOS model was established successfully. The expression intensity of TGF-β1 and CTGF in Oocytes of the PCOS groups was 9.545±2.954 and 9.665±2.400, respectively and was significantly higher than that of the control group 6.636±2.264 and 7.036±2.133; after treatment with rosiglitazone, the expression was significantly decreased 6.980±2.421 and 6.642±2.721 as compared with that of the model group (P〈0.05, P〈0.001). The values in serum of the PCOS groups were 3.749±2.054 and 0.265±0.129, and 1.914±1.801 and 0.096±0.088 in the control group which had statistically significant difference (P〈0.05, P〈0.O01). After treatment with rosiglitazone, the values were 2.3100±1.825 and 0.112±0.187 and were significantly different with those of the model group (P〈0.05, P〈0.O01). Conclusion TGF-β1 and CTGF play an important role in the development of ovary fibrosis in PCOS. However, RGZ may postpone the development of fibrosis by decreasing the levels of TGF-β1 and CTGF.
ISSN:0895-3988
2214-0190
DOI:10.3967/0895-3988.2012.01.007