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1.
Zhonghua Fu Chan Ke Za Zhi ; 42(8): 546-50, 2007 Aug.
Article in Chinese | MEDLINE | ID: mdl-17983495

ABSTRACT

OBJECTIVE: To investigate the effects of gonadotropin releasing hormone agonist (GnRH-a) and antagonist (GnRH-ant) on cyclophosphamide (CTX)-induced ovarian damage in rats. METHODS: Seventy-two Sprague-Dawley female rats were divided randomly into six groups, which received normal saline (NS), CTX, GnRH-a + NS, GnRH-a + CTX, GnRH-ant + NS, and GnRH-ant + CTX respectively. Levels of serum follicle-stimulating hormone (FSH), luteinizing hormone (LH) and estradiol (E(2)) were measured successively by the enzyme-linked immunosorbent assay method, and half of the rats were killed in the first week and between the fourth and the fifth week after stop of medication, respectively to compare the weight of the ovaries and the number of the primordial follicles and the growth follicles. RESULTS: (1) Throughout experiment, the serum levels of FSH, LH and E(2) of the control group fluctuated slightly, while those in the CTX group kept rising. During medication treatment, compared with the control group [(118 +/- 16) microg/L, (350 +/- 35) microg/L] and the CTX group [(113 +/- 15) microg/L, (289 +/- 42) microg/L], the concentrations of LH [(42 +/- 8) - (47 +/- 7) microg/L, (31 +/- 5) - (36 +/- 7) microg/L] and FSH [(124 +/- 45) - (136 +/- 32) microg/L, (178 +/- 54) - (198 +/- 27) microg/L] in the GnRH-a groups and the GnRH-ant groups were maintained at low levels significantly and the levels of LH in the GnRH-ant groups were significantly lower than that in the GnRH-a groups, but the levels of FSH in the GnRH-ant groups were significantly higher than that in the GnRH-a groups (P < 0.05); and extremely different from the GnRH-a groups [(0.98 +/- 0.18) - (1.46 +/- 0.22) ng/L], the level of E(2) of the GnRH-ant groups [(3.58 +/- 0.43) - (3.98 +/- 0.74) ng/L] did not significantly decrease (P < 0.01). After stop of therapy, the concentrations of LH, FSH and E(2) in the GnRH-a groups and the GnRH-ant + NS group rose gradually and were similar to the levels of the control group (P > 0.05), but the levels of FSH, LH and E(2) of the GnRH-ant + CTX group rose obviously and were similar to the levels of the CTX group, especially the FSH , and the levels of LH and FSH of the GnRH-ant + CTX group [(156 +/- 12) microg/L, (520 +/- 44) microg/L] and the CTX group [(178 +/- 18) microg/L, (546 +/- 36) microg/L] were significantly higher than that of the other four groups [(121 +/- 15) - (132 +/- 13) microg/L, (335 +/- 35) - (359 +/- 26) microg/L] at the 4(th) - 5(th) week after stop of treatment (P < 0.05). (2) At the 1(st) week after stopping therapy, the GnRH-a + NS group [(12 +/- 5) mg/100 g]and the GnRH-a + CTX group [(18 +/- 8) mg/100 g] had the lowest weight of ovaries which was significantly different from the other groups [(30 +/- 9) - (37 +/- 8) mg/100 g, P < 0.05]. At the 4(th) - 5(th) week after stopping therapy, the GnRH-ant + CTX group [(22 +/- 6) mg/100 g] and the CTX group [(20 +/- 4) mg/100 g] had the lowest weight of ovaries which were significantly different from the other groups [(29 +/- 5) - (31 +/- 9) mg/100 g, P < 0.05]. (3) At the 1(st) week after stopping therapy, there were the largest number of primordial follicles [(824 +/- 45), (689 +/- 39)] and the lowest number of growth follicles [(15 +/- 1), (21 +/- 3)] in the GnRH-a + NS group and the GnRH-a + CTX group, but there were the lowest number of primordial follicles [(255 +/- 24), (343 +/- 29)] and the largest number of growth follicles [(110 +/- 21), (87 +/- 17)] in the GnRH-ant + CTX group and the CTX group. At the 4(th) - 5(th) week after stopping therapy, the number of growth follicles in the GnRH-a + NS group (58 +/- 11) and the GnRH-a + CTX group (56 +/- 16) recovered to almost the level of the control group (57 +/- 9, P > 0.05), but the number of all kinds of follicles declined significantly in the GnRH-ant + CTX group [(195 +/- 15), (36 +/- 12)] and the CTX group [(212 +/- 11), (36 +/- 9)] compared to the other four groups [(302 +/- 15) - (690 +/- 43), (44 +/- 12) - (58 +/- 11), P < 0.05]. CONCLUSION: In rat model, GnRH-a prevents the ovarian function damage induced by CTX, but GnRH-ant does not show similar protective effect.


Subject(s)
Biomarkers/blood , Gonadotropin-Releasing Hormone/agonists , Gonadotropin-Releasing Hormone/antagonists & inhibitors , Ovary/physiopathology , Animals , Cyclophosphamide , Estradiol/blood , Female , Follicle Stimulating Hormone/blood , Luteinizing Hormone/blood , Ovarian Follicle/drug effects , Ovarian Follicle/physiopathology , Ovary/drug effects , Pituitary Gland/drug effects , Pituitary Gland/physiopathology , Random Allocation , Rats , Rats, Sprague-Dawley
2.
Zhonghua Fu Chan Ke Za Zhi ; 39(9): 591-4, 2004 Sep.
Article in Chinese | MEDLINE | ID: mdl-15498184

ABSTRACT

OBJECTIVE: To detect CD(36) expressions in polycystic ovary (PCO), and to explore its correlation with local androgen and insulin at transcription level. METHODS: From August 2002 to February 2003, 12 patients with asymmetric PCO, 15 primary or secondary infertile patients without endocrine disorders and 8 polycystic ovary syndrome (PCOS) with bilateral PCO were recruited. Extraction of follicular fluid and detection of testosterone (T), dehydroepiandrosterone sulfate (DHEAS), insulin (INS) and androstenedione (A(2)) were performed. Relative CD(36) mRNA expression level of human ovarian inner thecal cells was analyzed by auto image analysis system (IAS) after RT-PCR. RESULTS: The level of CD(36) mRNA expression in thecal cells was 0.24 +/- 0.07 in polycystic ovary of PCO group and 0.21 +/- 0.05 in bilateral ovaries of PCOS group, respectively, which were significantly lower than 0.83 +/- 0.13 in normal ovaries (P < 0.01). T and INS levels of follicle fluid in PCO were significantly higher than that in normal ovaries (P < 0.01). T and INS levels of follicle fluid were negatively related to CD(36) mRNA expression of follicular theca interna (r = -0.6810, r = -0.6708, P < 0.01). CONCLUSION: Decrease of scavenger receptor gene CD(36) mRNA may play a role in the pathogenesis of PCO by increasing the level of T and INS in follicular fluid.


Subject(s)
CD36 Antigens/biosynthesis , Insulin/metabolism , Ovary/metabolism , Polycystic Ovary Syndrome/metabolism , Testosterone/metabolism , Adult , Androstenedione/metabolism , CD36 Antigens/genetics , Female , Follicular Fluid/metabolism , Humans , Polycystic Ovary Syndrome/genetics , Polycystic Ovary Syndrome/immunology , RNA, Messenger/biosynthesis , Theca Cells/metabolism
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