Vascular endothelial growth factor [Vegf] localization in the mammary gland at various stages of its physiological cycle; a histological and immunohistochemical study

Vascular Endothelial Growth Factor [VEGF] is a potent angiogenic and vascular permeability enhancing factor under both physiological and pathological conditions including tumor angiogenesis. To study the localization and intensity of VEGF in the mammary gland at various stages of its physiological cycle. Mammary glands from sixty female albino rats were divided intosix groups [10 rats each]: Group I nulliparous, group II early pregnancy, group III late pregnancy, group IV lactating, group V early involution and group VI late involution. Human specimens from five females of variable age [childbearing and post-menopausal] were examined. Animal specimens were subjected to histological study while all specimens were subjected to immunohistochemical detection of VEGF. Morphometric analysis was performed for area% and optical density of positive VEGF reaction. VEGF was detected in epithelial lining of ducts and acini, endothelium of blood vessels as well as some stroma cells and macrophages. It was detected in resting nulliparous rat mammary gland with an increase during early pregnancy that became remarkable in late pregnancy and reached its maximum during lactation. Furthermore, VEGF was also detected in milk within lactating mammary acini. During involution, VEGF decreased progressively and reached a minimum in late involution. Human specimens showed stronger VEGF reaction during childbearing period than in post-menopause. The localization of VEGF in the endothelial cells of blood vessels, epithelium of mammary gland ducts and acini as well as some stroma cells and macrophages denoted that it is secreted by those cells. The increased VEGF in pregnancy and lactation indicates that it plays an important role in the development and function of the manunary gland

Histological assessment of the possible protective role of glimepiride against progression of experimentally induced diabetic nephropathy in rats

little is known about the potential effects induced by sulphonylureas independently of their anti-hyperglycemic action. The present study examined the effect of glimepiride treatment on the progression of renal histological changes in diabetic rats to determine whether therapeutic intervention with these agents would prevent the onset and progression of renal complications or not. forty-eight adult male albino rats were equally divided into four groups; control, normal rats receiving glimepiride, streptozotocin induced diabetic non-treated rats and glimepiride-treated diabetic rats. Blood glucose level measurement and histological evaluation of renal tissue elements using H and E, Masson trichrome, and PAS reaction techniques at four and eight weeks after treatment were performed. Stained sections were subjected to some morphometric measurements namely, glomerular tuft area [GTA], mesangial matrix index [MMI] and area per cent of connective tissue [CT]. Statistical analysis for significance of obtained data was performed using analysis of variance and student-T test. Glimepiride did not cause any histological renal impairment when used solely. Induction of diabetes had a significant negative impact on renal structure. In addition to significant elevation of blood glucose levels, increased kidney and kidney to body weight ratio was estimated. A variety of histological changes affecting the glomerular and tubular elements of renal tissue were detected and were more intense in the eighth week of the experiment. A significant increase in GTA, MMI and area per cent of C.T. were also found in diabetic rats. All the tested parameters showed a significant improvement in-the glimepiride-treated group. glimepiride could attenuate most of the histological changes produced in case of experimentally induced diabetic nephropathy in spite of persistent hyperglycemia. glimepiride could be used in Type I and type II diabetics to protect or slow down the progression of diabetic nephropathy

Effect of candesartan on cardiac and renal fibrosis induced by high salt intake in albino rats

High salt diet is independent determinant of left ventricular hypertrophy in addition to cardiac and renal fibrosis. Angiotensin II has possible role in mediating these deleterious effects. This work was designed to evaluate the possible effect of AT1 receptors blocker, candesartan on pathological change in heart and kidney induced by high salt diet [8%]. Materials and methods: High salt diet [8%] was administered to 30 male albino rats for eight weeks to induce left ventricular and renal hypertrophy and fibrosis. Candesartan in therapeutic equipotent dose in human [0.02mg/kg/day orally] was started one week before [prophylactic group] or five weeks after [curative group] starting high salt intake. By the end of eighth week from starting high salt diet intake, blood pressure was recorded rats were sacrified heart and kidney were removed, weighed and perpared for pathological examination. Results and Candesartan caused significant improvement in all parameters studied although the improvement was more evident in prophylactic than curative group. High salt intake [8%] induced hypertension, cardiac and renal hypertrophy with fibrosis in albino rats. These histological changes can be avoided or cured to a great extent by oral administration of AT1 blocker, candesartan. Angiotensin II may play a role in these deleterious changes induced by high salt diet