Effects of Genistein on Expressions of Bcl-2 and Bax mRNA in Ovarian Tissue of Polycystic Ovary Syndrome Rats

CHI Xiaoxing; ZHANG Mingyu; ZHANG Tao; ZHENG Lina; ZHANG Liyuan

doi:10.3969/j.issn.1006-267x.2014.04.034

Chinese Journal of Animal Nutrition >

2014 , Vol. 26 >Issue 4: 1120 - 1126

DOI: https://doi.org/10.3969/j.issn.1006-267x.2014.04.034

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Effects of Genistein on Expressions of Bcl-2 and Bax mRNA in Ovarian Tissue of Polycystic Ovary Syndrome Rats

CHI Xiaoxing ,
ZHANG Mingyu ,
ZHANG Tao ,
ZHENG Lina ,
ZHANG Liyuan

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1. College of Food Science, Heilongjiang Bayi Agricultural University, Daqing 163319, China;
2. Daqing Branch of Harbin Medical University, Daqing 163319, China

Received date: 2013-10-16

Online published: 2014-04-01

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Abstract

This experiment was conducted to study the effects of genistein (GEN) on the expressions of anti-apoptotic gene Bcl-2 mRNA and pro-apoptotic gene Bax mRNA in ovarian tissue of polycystic ovary syndrome (PCOS) rats. Ninety rats were divided into six groups: control group, model group, GEN low dose group, GEN middle dose group, GEN high dose group and estrogen group, respectively. The insulin combined with human chorionic gonadotropin molding method was used to establish PCOS animal models. After modeling, ten rats were selected from each group to carry out the test. The rats in dose groups were given 5, 10 and 20 mg/kg GEN, respectively, and the rats in estrogen group were given 0.5 mg/kg diethylstilbestrol. All compounds were administered intragastric administration on 15 consecutive days and observed a estrous cycle of 10 days. The expressions of Bcl-2 and Bax mRNA in rat ovarian tissue were examined by in situ hybridization. The activities of superoxide dismutase, catalase and glutathione peroxidase, and malondialdehyde content in rat ovarian tissue were determined. The results showed as follows: compared with PCOS model group, GEN could raise the expression of Bcl-2 mRNA and weaken the expression of Bax mRNA. And GEN could regulate the activities of antioxidant enzymes in rat ovarian tissue, which was as the same as the estrogen. In conclusion, GEN can enhance the expression of Bcl-2 mRNA and reduce the expression of Bax mRNA in rat ovarian tissue. It is presumed that it is one of the mechanisms of GEN improving ovarian function of PCOS.

Key words： genistein; polycystic ovary syndrome; ovary; Bcl-2 mRNA; Bax mRNA

Cite this article

CHI Xiaoxing , ZHANG Mingyu , ZHANG Tao , ZHENG Lina , ZHANG Liyuan . Effects of Genistein on Expressions of Bcl-2 and Bax mRNA in Ovarian Tissue of Polycystic Ovary Syndrome Rats[J]. Chinese Journal of Animal Nutrition, 2014 , 26(4) : 1120 -1126 . DOI: 10.3969/j.issn.1006-267x.2014.04.034

References

[1] AZZIZ R,SANCHEZ L A,KNOCHENHAUER E S,et al.Androgen excess in women:experience with over 1 000 consecutive patients[J].Journal of Clinical Endocrinology and Metabolism,2004,89(2):453-462.

[2] AZZIZ R.Controversy in clinical endocrinology:diagnosis of polycystic ovarian syndrome:the Rotterdam criteria are premature[J].Journal of Clinical Endocrinology and Metablism,2006,91(3):781-785.

[3] YANG J,LIU X S,BHLLA K,et al.Prevention of apoptosis by Bcl-2 release of cytochrome c from mitochondria blocked[J].Science,1997,275(5303):1129-1132.

[4] JAHANFAR S,EDEN J A,WARREN P,et al.A twin study of polycystic ovary syndrome[J].Fertility and Sterility,1995,63:478-486.

[5] EDEN J A.The polycystic ovary syndrome:a review[J].Australian and New Zealand Journal of Obstetrics and Gynaecology,1989,29(4):403-415.

[6] KOGISO M,SAKAI I,MITSUYA K,et al.Genistein suppresses antigen-specific competition with 17 beta-estradiol receptors for estrogen in ovalbumin-immunized BALB/c mice[J].Nutrition,2006,22(7/8):802-809.

[7] PORETSKY L,CLEMONS J,BOQOVICH K.Hyperinsulinemia and human chorionic gonadotropin synergistically promote the growth of ovarian follicular cysts in rats[J].Metabolism,1992,41(8):903-910.

[8] HSU S Y,HSUEH A J.Tissue-specific Bcl-2 protein partners in apoptosis:an ovarian paradigm[J].Physiological Reviews,2000,80(2):593-614.

[9] HUSSEIN M R.Apoptosis in the ovary:molecular mechanisms[J].Human Reproduction Update,2005,11(2):162-177.

[10] SLOT K A,VOORENDT M,DE BOER-BROUWER M,et al.Estrous cycle dependent changes in expression and distribution of Fas,Fas ligand,Bcl-2,Bax,and pro-and active caspase-3 in the rat ovary[J].Journal of Endocrinology,2006,188(2):179-192.

[11] JOHNSON A L,BRIDGHAM J T.Caspase-mediated apoptosis in the vertebrate ovary[J].Reproduction,2002,124(1):19-27.

[12] HSU S Y,LAI R J,FINEGOLD M,et al.Targeted overexpression of Bcl-2 in ovaries of transgenic mice leads to decreased follicle apoptosis,enhanced folliculogenesis,and increased germ cell tumorigenesis[J].Endocrinology,1996,137(11):4837-4843.

[13] 周东蕊, 杨利国, 姜勋平,等.外源bcl-2基因和脂质体对鸡卵泡颗粒细胞体外分裂和凋亡的影响.[J].南京农业大学学报,2001,24(2):75-78.

[14] MATHAI J P,GERMAIN M,SHORE G C.BH₃ only BIK regulates BAX,BAK-dependent release of Ca²⁺ from endoplasmic reticulum stores and mitochondrial apoptosis during stress-induced cell death[J].Journal of Biological Chemistry,2005,280(25):23829-23836.

[15] RANJAN P,BOSS J M.C/EBPbeta regulates TNF induced MnSOD expression and protection against apoptosis[J].Apoptosis,2006,11(10):1837-1849.

[16] MÉTRAILLER-RUCHONNET I,PAGANO A,CARNESECCHI S,et al.Bcl-2 protects against hyperoxia-induced apoptosis through inhibition of the mitochondria-dependent pathway[J].Free Radical Biology and Medicine,2007,42(7):1062-1074.

[17] KRAJEWSKI S,KRAJEWSKA M,SHABAIK A,et al.Immunohistochemical determination of in vivo distribution of Bax,a dominant inhibitor of Bcl-2[J].American Journal of Pathology,1994,145(6):1323-1336.

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