Histological and immunohistochemical study of nitric oxide synthase and effects of angiotensin receptor blockade in early phase of diabetes in rat kidney

Several studies have demonstrated that the pathophysiological and morphological changes in early diabetic nephropathy were mediated by an increase or decrease in nitric oxide [NO] production and/or activity. There are few reports suggesting a relationship between NO and the renin-angiotensin system. The present study was designed to determine the effects of early diabetic state on NO production and also to assess the possible effects of angiotensin receptor blockers [ARBs] on these changes. Thirty adult male albino rats were included in this study. Twenty were injected with streptozotocin for induction of diabetes. The other 10 were injected with the vehicle and served as control. Two days after injection, the diabetic animals were randomly divided into two groups of 10 animals each. One group was given valsartan as an ARB and the other group received no further treatment. Three weeks later, all animals were sacrificed and the kidneys were processed for obtaining paraffin sections. The sections were stained with H and E, Masson's trichrome, and periodic acid-Schiff. The sections were also stained with an immunohistochemical stain against endothelium-derived nitric oxide synthase [eNOS]. Diabetes induced histological changes in the form of glomerular hypertrophy, increased glomerular matrix, focal areas of tubular atrophy, medullary congestion, and slight fibrosis. Immunostaining was present in the control kidney in the glomeruli and in the collecting tubules of the medulla. Diabetes induced a positive reaction in the proximal and distal convoluted tubules and increased immunoreactivity in the collecting tubules. Treatment with valsartan resulted in an improvement in the morphology of the kidney and a reduction in the intensity of eNOS immunostaining. NO increases in early diabetic kidney and ARB in the form of valsartan could be recommended for preventing the development of diabetic nephropathy

Histological study on the effect of vitamin C on ischemia reperfusion injury in the adult rat ovary

Ovarian torsion may cause serious complications such as infertility in young women. Conservative management includes detorsion and reperfusion of the twisted segment. However, it may have local and systemic consequences due to production of large amounts of reactive oxygen species during reperfusion of ovaries. The present work aimed to study the possible histological and immunohistochemical changes due to ischemia-reperfusion injury in rat ovaries and the possible protective effect of vitamin C as an antioxidant. A total of 32 albino rats were divided into four groups. Group I was the control sham-operated group [either sham operated only, or with vitamin C administration]. In group II rats, ovarian ischemia was induced by torsion of the right adnexa. In rats of group III, 4 h of ischemia followed by reperfusion was performed. In rats of group IV, 4 h of ischemia was followed by 50 mg/kg vitamin C administration, which was injected intravenously, and then reperfusion was performed. Except for the ischemia group, all other groups were subdivided into two subgroups from which the right ovaries were surgically removed either after 5 h or after 2 weeks of starting the experiment. From the ischemia group ovarian samples were taken after 5 h only. Specimens were processed for paraffin sections and stained with H and E and with an immunohistochemical stain for apoptotic marker p53. Image analysis and statistical analysis of the obtained results were carried out. Severe vascular congestion, edema, hemorrhage, and increased P53 immunoreaction were detected in the ovaries after ischemia, which became less marked after reperfusion and considerably improved with vitamin C administration, especially after 2 weeks. Vitamin C treatment can help in protecting the ovaries from ischemia-reperfusion injury after detorsion

Immunohistochemical expression of vascular endothelial growth factor receptors FIt1 and KDR in the endometrium during the estrus cycle in albino rats

Angiogenesis is an important process in endometrial development and embryonic implantation and is regulated through vascular endothelial growth factor [VEGF]; its receptors Flt1 and KDR. This work aimed to study the immunoexpression of VEGF receptors [VEGF-Rs] in the endometrium at different ages and reproductive phases and correlate them with the histological profiles in these phases. Seventy female albino rats were included in this study. They were divided into seven groups of 10 rats each: one group consisted of rats in the prepubertal period at age 4-6 weeks; five groups consisted of rats in the reproductive period at age 6-10 months, which were divided according to estrus cycle phases into proestrus, estrus, metestrus, diestrus, and pregnant groups; and the sixth group consisted of rats in the postmenopausal period at age 15-18 months. The uteri of all rats were removed and processed for staining with H and E and were subjected to immunohistochemical staining for Flt1 and KDR. For morphometric measurements, uterine wall thickness and Flt1 and KDR optical density in the endometrial surface epithelium, glandular epithelium, stromal cells, and endometrial endothelial cells were measured using image analysis. Results were statistically compared. The expression of VEGF-Rs was highest in the pubertal age group with marked expression of these receptors in the proestrus phase followed by the estrus phase. This supports the role of sex hormones, especially the estrogen hormone, in regulating VEGF-R expression. The Flt1 receptor was predominantly expressed in endometrial and stromal cells as well as in blastocysts, whereas the KDR receptor was predominantly expressed in endometrial endothelial cells. Comparison among all groups and then between each two groups revealed statistically significant differences in the measured morphometric parameters. The upregulation of Flt1 and KDR could be involved in the regulation of endometrial endothelial cell proliferation and in increase in endometrial vascular permeability, especially at implantation sites

Effects of chronic estradiol treatment on the thyroid gland structure and function of ovariectomized rats

Estrogen therapy is widely used nowadays in women to treat many postmenopausal symptoms but it may have some undesirable effects due to multiple organs affection. The aim of this study was to determine the effects of chronic estradiol treatment oh the structure and function of the thyroid gland in ovarictomized rats as a model simulating menopause. Thirty adult female albino rats divided into three groups were used in this study, the first group was sham-operated, while the second and third groups were ovariectomized. The first and second groups were injected with olive oil while the third group was injected with estradiol diproprionate daily for three months, after that hormonal assay for T3, T4, TSH and histological specimens of the thyroid were taken and examined by light and electron microscopy. Serum levels of T3 and T4 were significantly decreased in ovariectomized animals and increased with estradiol treatment, while TSH increased in ovariectomized animals and decreased with estradiol. Histological and morphometric study in ovariectomized group revealed marked accumulation of colloid in follicular lumens with decreased epithelial height in addition to increased connective tissue amount while with estradiol treatment the follicles were smaller with small amount of colloid with increased epithelial height in addition to decreased connective tissue content. Ultrastructural study supported these results in addition to the presence of large amount of intracytoplasmic colloid vesicles after estradiol treatment. Decreased amount of estrogen may lead to thyroid hypofunction while estradiol treatment may lead to hyperactivity so it should be used very cautiously in the treatment of postmenopausal symptoms to avoid its undesirable stimulatory effect on the thyroid