Immunohistochemical evaluation of proliferation, apoptosis and steroidogenic enzymes in the ovary of rats with polycystic ovary

Abstract

ImmunohIstochemIcal evaluatIon of prolIferatIon, apoptosIs and steroIdogenIc enzymes In the ovary of rats wIth polycystIc ovary rev assoc med Bras 2014; 60(4):349-356 349original articleImmunohistochemical evaluation of proliferation, apoptosis and steroidogenic enzymes in the ovary of rats with polycystic ovary Conflict of interest: noneObjective: to evaluate the immunohistochemical expression of proliferative, apoptotic and steroidogenic enzyme markers in the ovaries of rats with polycystic ovary syndrome (PCOS). Methods: twenty rats were divided into two groups: GCtrl -estrous phase, and PCOS -with polycystic ovaries. The GCtrl animals were subjected to a lighting period from 7 am to 7 pm, while the animals with PCOS group remained with continuous lighting for 60 days. Subsequently, the animals were anesthetized, the ovaries were removed and fixed in 10% formaldehyde, prior to paraffin embedding. Sections were stained using H.E. or subjected to immunohistochemical methods for the detection of Ki-67, cleaved caspase-3, CYP11A1, CYP17A1 and CYP19A1. The results were analyzed using Student's t-test (p < 0,05). Results: morphological results showed evidence of interstitial cells originating from the inner theca cells of degenerating ovarian cysts in PCOS. Immunoexpression of Ki-67 was higher in the granulosa cells in GCtrl, and the theca interna cells in PCOS, while cleaved caspase-3 was higher in granulosa cells of ovarian cysts from PCOS and in the theca interna cells of GCtrl. Immunoreactivity of CYP11A1 in the theca interna, granulosa and interstitial cells was similar between the two groups, while CYP17A1 and CYP19A1 were higher in the granulosa and interstitial cells in the PCOS group. Conclusion: the results indicate that the interstitial cells are derived from the theca interna and that enzymatic changes occur in the theca interna and interstitial cells in ovaries of rats with PCOS, responsible for the high levels of androgens and estradiol.

Sex steroid receptors and apoptosis-related proteins are differentially expressed in polycystic ovaries of adult dogs

“…The administration of estradiol valerate as well as dihydrotestosterone and letrozole can mimic the syndrome as a result of metabolic and physiological disturbances and a sudden appearance of PCOs (Mahajan, 1988;Rezvanfar et al, 2014;Nikolić et al, 2015). Recently, Lombardi et al (2014) proposed a model of PCOs submitting rats to constant lighting at 400 lx for a period of 60 consecutive days. They observed persistent estrus, absence of corpora lutea and several ovarian cysts due to a fail in the preovulatory LH surge.…”

Vitamin D3 regulates steroidogenesis in granulosa cells through AMP‐activated protein kinase (AMPK) activation in a mouse model of polycystic ovary syndrome

“…38 Some of the published reports revealed the effects of vitamin D3 on the regulation of steroidogenesis pathway in human granulosa cells. 41,42 It is determined that androgen excess in hyperandrogenic PCOS women could disturb steroidogenesis pathway which subsequently leads to disruption in follicular development. Disturbance in this process could create ovulatory problems and infertility like that seen in PCOS women.…”

“…Disturbance in this process could create ovulatory problems and infertility like that seen in PCOS women. 41,42 It is determined that androgen excess in hyperandrogenic PCOS women could disturb steroidogenesis pathway which subsequently leads to disruption in follicular development. 3,43,44 In the present study, we induced PCOS mice model by DHEA to mimic the human anovulatory PCOS and investigated the mechanism of action of vitamin D3 on steroidogenesis process in granulosa cells of the polycystic ovary.…”

Effects of metformin on the adrenal cortex of androgenized rats

“…A rise in adrenocorticotropic hormone secretion can also be seen in PCOS, with increased production of corticosterone precursors and with steroidogenesis deviation, the latter manifesting as androgen production exclusively [21][22][23][24][25]. A rise in adrenocorticotropic hormone secretion can also be seen in PCOS, with increased production of corticosterone precursors and with steroidogenesis deviation, the latter manifesting as androgen production exclusively [21][22][23][24][25].…”