Effect of exogenous prostaglandin E2 administration on ovarian follicle growth and angiogenesis in rat with reference to pregnant mare serum gonadotrophin

Numerous evidences suggest a crucial role of prostaglandin E2 [PGE2] in ovarian function. In this study, the focus was to determine whether exogenous PGE2 administration could stimulate follicle growth, angiogenesis, and vascular endothelial growth factor [VEGF] expression, Immature female albino rats were injected once with normal saline, PGE2, or pregnant mare serum gonadotrophin and killed 24 h later. Samples were processed using paraffin blocks and sectioned for light microscopic examination. To evaluate follicle growth, counting and morphometric measurement of antral and ovulatory follicles were performed in serial ovarian sections using an image analyzer. To assess new vessel formation in ovarian follicles [follicular angiogenesis], an endothelial cell marker [anti CD34 antibody] and the immunofluorescent technique were used. Under an immunofluorescent microscope, enumeration of positive immune-stained endothelial cells [new microvessel] revealed the microvessel density. In addition, immunofluorescent staining with antibody against VEGF was performed for ovarian sections of the three groups. The study demonstrated that PGE2 markedly increased follicle counts and diameters versus the control. PGE2 mimicked pregnant mare serum gonadotrophin-induced follicle growth and showed a dramatic increase in follicular microvessel density versus control. Ovarian VEGF expression was not enhanced after PGE2 injection, Data presented in this study suggest that exogenous PGE2 could induce ovarian follicular growth and angiogenesis. PGE2 administration can be proposed to stimulate follicle growth in the clinical field. Elucidation of specific roles of factors involved in follicular growth may be useful in addressing the issue of infertility

Endometrial changes induced by prostaglandin E2 and EP4 receptor agonist in albino rats

Prostaglandin E2 [PGE2] plays a vital role in the endometrium at the initial phases of pregnancy in laboratory rodents. PGE2 exerts its effects by coupling to four subtypes of receptors designated as EP1, EP2, EP3, and EP4. Recently, a substance that acts specifically on the EP4 receptor was developed [EP4 receptor agonist=EP4A, APS-999 Na]. Endometrial stromal collagen I, total glycosaminoglycans, hyaluronic acid, and CD44 molecule are commonly subjected to drastic changes at the implantation window. This study was conducted to investigate changes in the expression of these components after administration of PGE2 and the EP4A in rat. Immature female albino rats were injected once with normal saline, 50microg of PGE2, of 50microg of EP4A and killed 24 h later. Light microscopy and immunohistochemistry were used in this study. The study results revealed fraying and disintegration of stromal collagen I; accumulation of matrix glycosaminoglycans and hyaluronic acid after PGE2 as well as EP4A injections compared with the control. In addition, EP4A and PGE2 induced the expression of the molecule CD44 on the endometrial luminal and glandular epithelia Edema of the endometrial stroma was obtained after PGE2 and EP4A treatments. This study revealed that PGE2 and EP4A enhanced endometrial factors that are essential for the success of the implantation process. As long as EP4A produced similar effects to PGE2, it could be concluded that PGE2 mediated these actions partially through the EP4 receptor. PGE2 and EP4A may prove to be promising tools for implantation disorders in the clinical field

Structural characteristics of the rat visceral yolk sac during early pregnancy with emphasis on hematopoietic cells

The yolk sac is the first definitive fetal membrane of vertebrates. During embryonic development, hematopoiesis begins first in the yolk sac. This study was carried out to investigate the ultrastructural characteristics of the early rat extraembryonic visceral yolk sac membrane and hematopoietic cells localized in the yolk sac vitelline vessels. Pregnant albino rats were killed at gestational days 10-12. Yolk sac specimens were processed for light, transmission, and scanning electron microscopic examination. The study demonstrated the microscopic structure of the yolk sac membrane and the different hematopoietic cells in yolk sac vitelline vessels at this stage of gestation. The endoderm cells revealed a cytoplasm rich in cell organelles characteristic of endocytosis, phagocytosis, and active protein synthesis, as well as cell junctions between adjacent cells. The apices of the endoderm cells revealed numerous microvilli of two types and a whitish coat on top of the cells. In yolk sac vitelline vessels, a large number of blood cells were seen. Many cells were at different stages of mitosis. Ultrastructurally, blast cells including immature differentiating erythroblasts were recognized, together with a few mature erythrocytes. Furthermore, mature lymphocytes were also seen in vitelline vessels on gestational day 12. Yolk sac lymphocytes revealed a morphology typical of peripheral blood lymphocytes. This study demonstrated the importance of the yolk sac for adequate embryonic nourishment, as well as different blood elements necessary for potent immune response. The location of mature lymphocytes inside vitelline vessels suggests a possible emergence from the yolk sac membrane. However, future studies are needed to explore the exact origin of these cells

Evaluation of honey protective effect on lead induced oxidative stress in rats

Lead toxicity is a worldwide health problem due to continuous exposure of the population to lead in the environment especially workers in industries. It affects many body organs especially the liver and kidneys. The aim of this study is to investigate the protective effect of natural honey against lead induced oxidative stress, hepatotoxicity and nephrotoxicity. Forty male albino rats were used in this study divided into 4 equal groups. Group [I] the control group were given distilled water orally for 4 weeks. Group [II] rats were given 1.5 ml/kg natural honey orally for 4 weeks. Group [III] rats were given lead acetate [0.2%] in drinking water for 4 weeks .Group [IV] rats were given lead acetate [0.2%] in drinking water and 1.5 ml/kg natural honey orally for 4 weeks. Blood and tissue samples were taken after four weeks. Lipid peroxidation product, malondialdehyde [MDA] in plasma, liver and kidney were determined, blood glutathione peroxidase activity [GPx] and serum nitric oxide [NO] levels were also measured, Liver function tests [serum alkaline phosphatase [ALP], aspartate transaminase [AST] and alanine transaminase[ALT] were measured. Kidney function tests [blood urea and s. creatinine] were estimated. Histopathological examination of liver and kidney sections was performed. showed significant [P>0.01] increase in the mean MDA of plasma. liver and kidney of lead acetate group [Group III] with decreased antioxidant enzyme activity [GPx] activity and [NO] and increase levels of AST, ALT, ALP, urea and serum creatinine together with histopathological changes in liver and kidney sections. Honey alleviated the increased MDA levels, and ameliorate the elevated AST, ALT, ALP, urea and serum creatinine in the combination group. The present study revealed that natural honey could diminish the adverse effects of lead acetate as shown in the histological analysis of rat livers and kidneys. The present results indicated that natural honey can modulate the damage in liver and kidney cells from oxidative stress induced by lead toxicity in tart