Alterations in hippocampal neurogenesis and hippocampal insulin signaling pathway in rat with metabolic syndrome.

Objectives: We aimed to examine the level of hippocampal neurogenesis, and assess learning and anxiety and the level of some proteins involving insulin signaling pathways in rats with Metabolic Syndrome (MetS); and to reveal the relationship among them. Materials and Methods: Totally, 30 Wistar-albino rats were used. The rats were divided into three groups: Control, MetS, and MetS+Ins. Immunohistochemical staining was performed to evaluate the levels of neurogenesis markers; Doublecortin (DCX), Neuronal-Differentiation-1 (NeuroD1), Ki67, and Neuronal nuclear protein (NeuN). Then, cleaved caspase-3 and TUNEL labeling were performed to detect the level of apoptosis. Additionally, behavior tests were performed to evaluate the learning-memory levels and anxiety-like behaviors. Insulin, Insulin Receptor (IR), Insulin Receptor Substrate (IRS2), glucose transporter (GLUT)-3, and GLUT4 protein expression levels were analyzed to evaluate the possible changes in the insulin signaling pathway. Results: An increase in anxiety with memory deficiency was observed in MetS. In the hippocampus of MetS, an increase was detected in the level of apoptosis, whereas a decrease was detected in the expression level of the neurogenesis marker. Insulin secretion and IR levels decreased in hippocampal neurons. We observed that GLUT3 and GLUT4 levels increased because of the non-activated insulin signaling pathway. Conclusion: We think that the insulin signaling pathway may have an effect on the decreased neurogenesis in the MetS group. So, the evaluation of the Mitogen-activated protein kinase (MAPK) pathway and the investigation of the effect of endoplasmic reticulum stress on this pathway will be among the targets of our future studies.

Effects of aerobic exercise on lipopolysaccharide-induced experimental acute lung injury in the animal model of type 1 diabetes mellitus.

NEW FINDINGS: What is the central question of this study? We evaluated the effects of diabetes and exercise on lipopolysaccharide-induced acute lung injury. By providing a comprehensive analysis of redox status, blood gases and histological parameters, we aimed to contribute to the ongoing debate in the literature. What are the main findings and its importance? We demonstrated the preventive effect of exercise, but diabetes did not alter the severity of acute lung injury. ABSTRACT: Acute lung injury (ALI) is a life-threatening respiratory condition. Diabetes (DM) is a metabolic disease characterized by hyperglycaemia. There is an ongoing debate concerning whether there is a protective effect of diabetes in ALI. Exercise is a special type of physical activity that has numerous beneficial effects. The aim of our study was to investigate the effects of diabetes and exercise on the prognosis of ALI. Male Wistar albino rats were divided into two groups (sedentary and exercise). Both groups were divided into four subgroups: Control, ALI, DM, DM+ALI (n = 6 each). Diabetes was induced by injection of streptozotocin (50 mg/kg i.p.). The maximal exercise capacity was determined with the incremental load test. Animals were exercised on a treadmill for 45 min at 70% of maximal exercise capacity, 5 days a week for 12 weeks. Acute lung injury was induced by intratracheal injection of lipopolysaccharide (100 µg/100 g body weight) 24 h before the end of the experiment. We performed arterial blood gas analysis. Redox status was measured in both plasma and lung tissue. Malondialdehyde and 8-hydroxy-2'-deoxyguanosine levels were measured in lung tissue. Lung tissue was evaluated histologically. Acute lung injury caused significant damage in the lung tissue, which was verified histologically, with an increase in oxidative stress parameters. Exercise prevented the lung damage induced by ALI and reduced oxidative stress in the lung tissue. Diabetes did not alter the magnitude of damage done by ALI. Exercise showed a protective effect against DM and ALI in rats. The effect of DM was insignificant for the prognosis of ALI.

Evaluation of blood-testis barrier integrity in terms of adhesion molecules in nonobstructive azoospermia.

Blood-testis barrier (BTB) is critical for maintaining fertility. The integrity of tight junctions (TJs) provides restricted permeability of BTB. The aim of this study was to evaluate the relationship between BTB and Sertoli cells. Testicular sperm extraction (TESE) obtained from nonobstructive azoospermia (NOA) patients was examined: Group I (spermatozoa+) and Group II (spermatozoa-). The tissues were stained with haematoxylin eosin, periodic acid-Schiff and Masson's trichrome for Johnsen's score evaluation. Apoptosis and adhesion molecules such as claudin-11, occludin and ZO-1 were assessed. In Group I, the integrity of the seminiferous tubules was intact. In Group II, some seminiferous tubule walls were lined only with Sertoli cells, had a thickening of the basement membrane, and oedema in interstitial spaces. In Group I, the seminiferous tubule consisted of a stratified columnar epithelium, claudin-11 expressions were observed as linear staining in the basal zone of the tubule, while seminiferous tubules, with low epithelium, displayed a punctate type of staining. Immunohistochemical observations were consistent with the ultrastructural findings. In Group II, high apoptosis and unstained/irregular TJ formation in claudin-11, occludin and ZO-1 were observed. In conclusion, disruption of relation between BTB and TJs may reveal inadequate spermatogenesis, which is one of the mechanisms behind azoospermia.

Targeting Apoptosis Through Foxp1, and N-cadherin with Glatiramer Acetate in Chick Embryos During Neural Tube Development.

AIM: To demonstrate the effect of glatiramer acetate (GA) in chick embryos on neural tube (NT) development, and to explore its effects of Foxp1, apoptosis, and N-cadherin. MATERIAL AND METHODS: One hundred fertile, specific pathogen free eggs were divided into 5 groups for this study. The eggshell was windowed specifically at 24 hours of incubation. The embryos in Group 1 (n=20) were treated with 10 µl physiological saline; in Group 2 the embryos (n=20) were given 10 µl GA (equal to daily human therapeutic dose); 20 µl GA (equal to twice daily human therapeutic dose) was injected to embryos in Group 3 (n=20); in Group 4 and 5, 30 µl and 40 µl GA were administered to the embryos (n=20) (equal to x3 and x4 daily human therapeutic dose, respectively). Each egg was re-incubated for 24 hours more. Then, histological and immunohistochemical evaluation of the subjects were done. RESULTS: The embryos with NT defect showed FOXP1 expression without N- cadherin or staining with N-cadherin in another location in our study. We interpreted this result as GA leading to an NT closure defect by increasing FOXP expression. Moreover, we also showed the reverse relation between FOXP1 and N-cadherin at the immunohistochemical level for the first time. CONCLUSION: GA affects the spinal cord development through FOXP in the chick embryo model at high doses.

A laboratory modification to testicular sperm preparation technique improves spermatogenic cell yield.

Testicular sperm extraction is a common procedure used to find spermatogenic cells in men with nonobstructive azoospermia. The laboratory processing of biopsied testicular tissues needs to be performed meticulously to acquire a high yield of cells. In this study, the effectiveness of mincing the tissues after testicular biopsy was assessed using histological evaluation, as was the possible adverse effect of residual tissue on the migration of spermatogenic cells during density gradient centrifugation. Our results indicate that testicular residual tissue, when laid on the density gradient medium along with the sperm wash, hinders the spermatogenic cells' forming a pellet during centrifugation, and therefore impairs the intracytoplasmic sperm injection procedure. Whereas the mean number of recovered cells from the sperm wash medium (SWM) with residual tissue is 39.435 ± 24.849, it was notably higher (60.189 ± 28.214 cells) in the SWM without minced tissues. The remaining tissue contained no functional seminiferous tubules or spermatogenic cells in histological sections. In conclusion, the remaining residual tissue after mincing biopsied testicular tissue does not add any functional or cellular contribution to spermatogenic cell retrieval; in fact, it may block the cellular elements in the accompanying cell suspension from migrating through the gradient layers to form a pellet during centrifugation and cause loss of spermatogenic cells.