共查询到20条相似文献，搜索用时 15 毫秒
1.
Eduardo Fernandes Bondan Maria de Fátima Monteiro Martins Deborah Eileen Menezes Baliellas Caio Fernando Monteiro Gimenez Sandra Castro Poppe Maria Martha Bernardi 《Microscopy research and technique》2014,77(1):23-30
Propentofylline (PPF) is a xanthine derivative with pharmacological effects distinct from those of the classical methylxanthines. It depresses activation of microglial cells and astrocytes which is associated with neuronal damage during neural inflammation and hypoxia. The aim of this study was to evaluate whether PPF had the capacity of affecting glial cells behavior during the process of demyelination and remyelination following ethidium bromide (EB) gliotoxic injury. EB injection into the CNS is commonly used as an experimental demyelinating model inducing local oligodendroglial and astrocytic death, which results in primary demyelination, blood–brain barrier and glia limitans disruption and Schwann cells invasion. Sixty Wistar rats were divided into four different groups receiving 10 microlitres of 0.1% EB or 0.9% saline solution into the cisterna pontis and treated or not with the xanthine. PPF treatment was done using 12.5 mg/kg/day by the intraperitonial route for 31 days of the experimental period. The rats were euthanized from 7 to 31 days after EB injection and brainstem sections were collected and processed for light and transmission electron microscopy studies. Results from both groups were compared by using a semi‐quantitative method developed for documenting in semithin sections the extent and nature of remyelination of demyelinating lesions. Results showed that PPF administration after EB injection significantly increased both oligodendroglial and Schwann cell remyelination at 31 days (mean remyelination scores of 3.67 ± 0.5 for oligodendrocytes and 1.27 ± 0.49 for Schwann cells) compared to untreated animals (scores of 3.19 ± 0.57 and 0.90 ± 0.33, respectively). Microsc. Res. Tech. 77:23–30, 2014. © 2013 Wiley Periodicals, Inc. 相似文献
2.
A differential morphological response of mature oligodendrocytes (OL) isolated from human and pig brains to the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) and to the nerve growth factor (NGF) was observed. In both cases, OL regenerate their processes; however, the rate and the extension of the process formation of human OL were behind that of pig OL. Presumably, the advanced age of the human tissue in these experiments might have contributed to this decrease in process formation, an effect that was already observed for rat OL [Yong et al. (1991) J Neurosci Res 29:87-99]. The less effectivity of NGF via TrkA, which was immunocytochemically shown in human OL, and of TPA via the protein kinase C (PKC) pathway, may have its common focus on the mitogen-activated protein kinase (MAPK) cascade. In this context, it was noted that only a few studies on aging of mature OL are available. It is conceivable that age-related changes in the properties of OL could be an important factor for their cellular responsiveness during longer lasting demyelinating diseases such as multiple sclerosis. Hence, this review would like to provide a basis for future investigations on the aging of mature OL. The data presently available suggest a preliminary classification of mature OL into three categories. 相似文献
3.
探讨流式细胞术在检测高糖诱导的早期雪旺细胞凋亡中应用。选用培养大鼠的雪旺细胞,将细胞分为正常对照组(5.6mmol/L葡萄糖),高糖组(50mmol/L葡萄糖),高渗出组(50mmg/L甘露醇),培养7天后,收集细胞。48h后应用流式细胞术采用Annexin-V/PI检测法和JC-1检测早期细胞的细胞膜凋亡率和线粒体膜电位变化。结果表明:高糖与正常糖浓度处理的雪旺细胞比较,高浓度葡萄糖诱导雪旺凋亡率明显高于正常葡萄组的凋亡率,线粒体膜电位明显高于正常对照组。高渗透组与正常对照组凋亡率及线粒体无明显升高。通过采用流式细胞细胞术结合单克隆抗体,能够快速、灵敏和准确检测雪旺细胞在细胞膜的通透性改变和线粒体膜电位变化。为研究雪旺细胞凋亡提供客观、直接、准确的方法。 相似文献
4.
Some studies indicate that diabetes mellitus exerts an influence on the gastrointestinal tract and its diffuse neuroendocrine system (DNES) in regard to cellular density and neuroendocrine content. Since there is no data about relationship between experimentally induced non–insulin‐dependent (type 2) diabetes mellitus (NIDDM) on the gut K cells, the aim of our study was to investigate immunohistochemical, stereological and ultrastructural changes of rat K cells after 12 days of dexamethasone treatment. Twenty male Wistar rats aged 30 days were given daily intraperitoneally 2 mg kg–1 dexamethasone (group DEX, 10 rats) or saline (group C, 10 rats) for 12 days. Tissue specimens were obtained from each antrum with corpus and different parts of the small (SI) and large intestine (LI) of all animals. Immunohistochemistry was carried out using antisera against the GIP and insulin. Transmission electron microscopy was also used. Although, according to the literature data, rat K cells are present in the duodenum and jejunum and, to a lesser extent, in the ileum, in the present study we observed that those cells were abundant also in all parts of the LI. We observed generally that GIP‐producing K cells were augmented in all parts of SI and decreased in the LI of DEX rats. Insulin immunoreactivity (ir) coexpressed with GIP‐ir in K cells and was stronger in the SI of DEX rats as compared with C rats. We also found by electron microscopy that small intestinal K cells have features not only of GIP‐secreted but also of insulin‐secreted cells. We concluded that dexamethasone treatment caused proliferation of K cells in the rat SI, and simultaneously transformation of GIP‐producing K cells to insulin‐synthesizing cells. 相似文献
5.
Maximiliano GIRAUD-BILLOUD Claudio M. FADER Rocío AGÜERO Fernando EZQUER Marcelo EZQUER 《Biocell》2018,42(2):35-40
Diabetic nephropathy (DN) is the most frequent cause of chronic renal failure. Until now, thepathophysiological mechanisms that determine its development and progression have not yet been elucidated. In thepresent study, we evaluate the role of autophagy at early stages of DN, induced in type 2 diabetes mellitus (T2DM)mouse, and its association with proximal tubule membrane endocytic receptors, megalin and cubilin. In T2DManimals we observed a tubule-interstitial injury with significantly increased levels of urinary GGT and ALP, but anabsence of tubulointerstitial fibrosis. Kidney proximal tubule cells of T2DM animals showed autophagic vesicleslarger than those observed in the control group, and an increase in the number of these vesicles marked with LBPAby immunofluorescence. Furthermore, a significant decrease in the ratio of LC3II/LC3I isoforms and in p62 proteinexpression in DN affected animals is shown. Finally, we observed a marked increase in urinary albumin and vitamin Dbinding-protein levels in T2DM animals as well as a significant decrease in expression of megalin in the renal cortex.These results indicate an alteration of the tubular endocytic transporters in DN, which could be related to autophagicdysfunction, which would in turn result in impaired organelle recycling, thus contributing to the progression of thisdisease. 相似文献
6.
Benedicto HG Bombonato PP Macchiarelli G Stifano G Prado IM 《Microscopy research and technique》2011,74(11):1018-1023
The heart is composed by a specialized muscle, whose form and function are essentials for an adequate work and shows an amount of connective tissue which support and provide insertion for this muscle, whose collagen fibers are responsible for determination of tissue feature. Our objective was to identify the structural arrangement of the heart collagen fibers in dogs. The hearts of the dogs were submitted to the process of the controlled digestion with NaOH solution and observed by scanning electron microscope. Our results showed that the collagen fibers of the endomysial wall have structural arrangement composed by an irregular network with one layer in normal dogs but in diabetic dogs the network acquires a greater amount of the fibers and layers, looking like a \"rug\" of fibers modifying the relationships of the stress/strain of the tissue. Ahead of the observed results we are able to conclude that exist increase in the amount and thickness of cardiac collagen fibers, beyond the increase of layers and architectural disarrangement in the endomysial wall in the diabetic dogs. 相似文献
7.
Marli Aparecida dos Santos Pereira Maria Claúdia Bagatin Jacqueline Nelisis Zanoni 《Biocell》2006,30(2):295-300
We assessed the ascorbic acid (AA) supplementation on the myenteric neurons in the duodenum of rats. Fifteen rats with 90 days of age were divided into three groups: control (C), diabetics (D) and ascorbic acid treated diabetics (DA). After 120 days of daily treatment with AA, the duodenum was submitted to the NADH-diaphorase (NADH-d) histochemical technique, which allowed us to evaluate the neuronal density in an area of 8.96 mm2 for each duodenum, and also to measure the cellular profile area of 500 neurons per group. The supplementation promoted an increase on AA levels. The neuronal density (p < 0.05) was higher in the group DA when compared to group D. There were no significant differences in the neuronal areas, when we compared groups C (204 +/- 16.5) and D (146.3 +/- 35.84) to groups D and DA (184.5 +/- 5.6) (p > 0.05). The AA-supplementation avoided the density reduction of the NADHd myenteric neurons in the duodenum of diabetic rats. 相似文献
8.
The literature concerning Schwann cells (SCs) and macrophages in myelin phagocytosis during Wallerian degeneration is reviewed. SCs carry out the first step in the removal of myelin by segmenting myelin and then incorporating the degraded myelin. The recruited macrophages then join in the myelin-phagocytosis event, appearing to make full use of their original phagocyte abilities until the end of myelin clearance. The molecular mechanisms of the two cells underlying myelin phagocytosis are thought to be different; myelin phagocytosis by SCs being lectin-mediated, i.e., opsonin-independent, whereas that of macrophages is mainly opsonin-dependent. It is important to note that SCs and macrophages cooperatively accomplish myelin phagocytosis. 相似文献
10.
The objective of this work was to evaluate the effect of the ascorbic acid supplementation on the cellular proliferation on the ileum mucosa of diabetic rats. Fifteen 90-days rats were divided in the groups: control, diabetic and diabetic supplemented with ascorbic acid (DA). Two hours prior the sacrifice, they were injected with Vincristin. Semi-seriate histological cuts stained with HE were accomplished. About 2500 crypt cells from the intestinal mucosa were counted in order to obtain the metaphasic indexes. The height and depth of 30 villi and 30 crypts were measured for each animal, respectively. The metaphasic indexes showed no significant changes when we compared the three groups: 20.2 +/- 0.7 (control), 18 +/- 1.9 (diabetic) and 17 +/- 1.4 (DA) (p > 0.05). The values obtained from the crypts measurement were 221.2 +/- 8.5 (control), 225.3 +/- 9.5 (diabetic) and 222 +/- 34 (DA). The villi of the control, diabetic and DA animals presented the following results: 301.7 +/- 25.33, 304.8 +/- 25.63 and 322.1 +/- 45.77 respectively. The morphometric data were not different statistically (p > 0.05). Summing up, the present work showed that there was no alteration in the cellular proliferation of the ileum of diabetic-induced rats supplemented with ascorbic acid. 相似文献
11.
This work aimed to clarify the interaction between the fetus and pregnant patients with gestational diabetes mellitus (GDM), the lipid metabolomics analysis of the fetal umbilical cord blood of GDM patients and normal pregnant women were performed to screen out the specific lipid metabolites for pathogenesis of GDM. From 2019–2020, 21 patients with GDM and 22 normal pregnant women were enrolled in Hexian Memorial Hospital, Panyu District, Guangzhou. The general information such as weight, height, age, body mass index (BMI) before pregnancy were analyzed. Non-targeted metabonomic detection and analysis were performed in umbilical cord plasma using LC-MS method. The age, BMI, delivery methods, and infant weight were different between GDM and control. There were 167 lipid metabolites in umbilical cord blood associated with GDM. Among them, 158 upregulated and 9 downregulated in GDM. There were 13 dysregulated metabolites with C < 30, including Lyso-phosphatidyl-colines LPC 16:0, 18:2, 18:1, 18:0, 20:4 and 22:6, glycerophosphocholines PC O-16:1, oleoylcarnitine CAR 18:2 and 18:1, dihexosylceramides Hex2Cer 13:0;2O, phosphatidylethanolamine PE O-22:6_2:0 and PE O-22:6_3:0 and sphingomyelin SM 8:0; 2O/11:0. Those metabolites were associated with glycerophospholipid metabolism and sphingolipid metabolism. Therefore, Lyso-phosphatidyl-colines, glycerophosphocholines, oleoylcarnitine, dihexosylceramides, phosphatidylethanolamine, and sphingomyelin were main lipid metabolites of GDM, which might be used for diagnosis and treatment of GDM. 相似文献
12.
In this study we investigated the effects of severe hypothermia (cryoinjury) on oligodendrocyte (OL) cell marker expression and morphological features. We used a chemically defined cell culture medium, glial development medium (GDM), which favored the optimal expression of the OL phenotype in CG4 cells. Experiments using CG4 cells cultured in 2% serum or in GDM were conducted in parallel. After severe hypothermia, cells were reanimated at 37 degrees C and 4.5% CO(2) and cultured in either GDM or in medium supplemented with 2% serum. In either medium, around 70% of the total number of cells detached within 2 to 4 hours following reanimation. Oligodendroglial markers such as A2B5, O4, Tf, ferritin, tubulin, and MBP were examined by double and triple immunofluorescence. All of these markers except MBP re-appeared at different times during the recovery period for up to 48 hours. Glial fibrillary acidic protein (GFAP) and heat shock protein 60 (HSP-60) were used as injury markers. The presence of serum induced HSP-60 expression, while GDM did not. All CG4 cells expressed HSP-60 in response to hypothermia independently of the cell culture medium used. Cryoinjury induced a spectrum of morphological changes in CG4 cells. The expression of OL specific markers was also influenced by hypothermia. Moreover both, serum and cryoinjury induced the expression of HSP-60 that colocalized with OL and myelin markers. The expression of GFAP by injured cells but not by normal cells corroborated the state of injury of CG4 cells. 相似文献
13.
Metidieri HT Mancio RD Mayoral ÉE Rojas FA Peroni LA Ferri AT Lourenço EA Caldeira EJ 《Microscopy research and technique》2012,75(7):928-934
Background: Diabetes mellitus results in many complications, also compromising the salivary glands. The current treatment for this condition should be a substituting method to exogenous insulin. In this aspect, the immunotherapy has been tested, but, it can be inefficient as an agent for the control of damage caused by diabetes. Thus, the aim of this study was to evaluate the anti‐CD3 monoclonal antibody as alternative immunotherapy in the recovery of salivary glands of spontaneously diabetic NOD (nonobese diabetic) mice. Methods: NOD mice were divided into two groups of 10 animals: group I (untreated diabetic mice) and group II (anti‐CD3‐treated diabetic mice). After treatment, the samples of salivary glands were collected for histological examination under both transmitted and polarized light microscopy. Results: Alterations in tissue architecture; increase in extracellular matrix and presence of inflammatory process were observed in untreated animals. Recovery of the salivary acinar cells occurred in treated animals. The parotid glands demonstrated a smaller amount of collagen fibers and were not observed severe inflammatory processes. Conclusion: These results indicate that immunotherapy contributed to reestablishment of tissue damaged by the hyperglycemic condition, demonstrating that the immunomodulation plays an important role in the recovery of salivary glands. Microsc. Res. Tech., 2012. © 2012 Wiley Periodicals, Inc. 相似文献
14.
Multiple sclerosis (MS) is an inflammatory disorder of the central nervous system (CNS), characterised by focal destruction of myelin. Although it is evident that the immune system contributes to tissue destruction in MS, it is still unclear as to whether this immune response is a cause or a consequence of the disease process. In addition, there is debate over the contribution of axonal damage to clinical progression. We have described a murine model of relapsing-remitting MS (RR-MS), the most common form of the disease, following immunisation with the myelin component, myelin oligodendrocyte glycoprotein (MOG). We showed that a single injection of a MOG peptide (MOG(35-55)) in NOD/Lt mice induces a paralytic relapsing disease with extensive plaque-like demyelination. This model also mimics many of the immunological features associated with RR-MS. To investigate the relationship between clinical episodes, inflammation, and demyelination/remyelination, we analysed lesions during each attack and remission over the course of the disease, using histological, immunocytochemical, and electron microscopy (EM) techniques. We show that morphological features of lesions in our model resemble those observed in MS. Indeed, severe inflammation and demyelination coincide with the peak of clinical episodes while remissions are characterised by quiescent plaques. Furthermore, axonal damage is evident from the earliest stage of the disease and increases in severity with subsequent relapses. These data establish that in the model of MS-like disease, the peak of clinical episodes coincides with severe inflammation and demyelination and that axonal pathology correlates with clinical progression. 相似文献
15.
16.
Ryuji Fujihara Yoichi Chiba Toshitaka Nakagawa Nozomu Nishi Ryuta Murakami Koichi Matsumoto Machi Kawauchi Tetsuji Yamamoto Masaki Ueno 《Microscopy research and technique》2016,79(9):833-837
Their aim was to examine whether microvascular leakage of endogenous albumin, a representative marker for blood–brain barrier (BBB) damage, was induced in the periventricular area of diabetic db/db mice because periventricular white matter hyperintensity formation in magnetic resonance images was accelerating in elderly patients with diabetes mellitus. Using light and electron microscopes, and semi‐quantitative analysis techniques, immunoreactivity of endogenous albumin, indicating vascular permeability, was examined in the periventricular area and spinal cord of db/db mice and db/+m control mice. Greater immunoreactivity of albumin was observed in the vessel wall of the periventricular area of db/db mice than in controls. Additionally, weak immunoreactivity was observed in the spinal cord of both db/db mice and controls. The number of gold particles, indicating immunoreactivity of albumin, in the perivascular area of db/db mice was significantly higher than that of control mice, but there was no significant difference in the number of particles in the spinal cord between db/db mice and controls. These findings suggest that albumin microvascular leakage, or BBB breakdown, is induced in the periventricular area of diabetic mice. Microsc. Res. Tech. 79:833–837, 2016. © 2016 Wiley Periodicals, Inc. 相似文献
17.
18.
Adrenomedullin (AM) is a multiregulatory peptide which is expressed in a wide range of tissues. In the pancreas, AM was first found in mammals, including man, and its colocalization with the pancreatic polypeptide (PP) was established in islet F cells. In addition, three different AM receptors have been characterized in B-cells. AM has been also located in the pancreatic cells of other vertebrate classes. The frequency and distribution of AM cells vary between different animals; they can be found scattered among the exocrine tissue, in the islets, or in ductal epithelia. The colocalization of AM with other hormones presents different patterns, although in birds, as in mammals, it seems to colocalize only with PP. The best-determined pancreatic AM function is the inhibition of insulin secretion in B-cells, which seems to be linked to a recently discovered binding protein, factor H. In relation to this physiological role, clinical data show that AM is raised in some groups of both types I and II diabetic patients and AM might have triggered the disease in a subset of them. On the other hand, AM pancreatic cells are also involved in the response to septic shock by increasing AM circulating levels. A third putative function is the inhibition of amylase secretion by the exocrine pancreatic cells. AM has been found in embryonic mammalian pancreas from the earliest stages of the development, colocalizing with all pancreatic hormones, although in adults only coexpression with PP is kept. AM may play a role in the growth and morphogenesis of the pancreas. 相似文献
19.
We have used rat sciatic nerves submitted to freezing and freeze‐fracture to determine the elemental composition of small domains of the peripheral nerve studied at high resolution by scanning electron microscopy. We found that myelin of Schwann cells is unique in its high content in phosphorus (P) that was more than 10 times higher than P measured in any other cells. This high concentration in P makes myelin chemistry suitable of monitoring at the subcellular level using the herein described methodology. Microsc. Res. Tech. 78:537–539, 2015. © 2015 Wiley Periodicals, Inc. 相似文献
20.
YUEHUA SHI QIUYING YAN QIN LI WEI QIAN DONGYAN QIAO DONGDONG SUN HONG YU 《Biocell》2023,47(1):165-173
The placenta plays an important role in nutrient transport to maintain the growth and development of theembryo. Gestational diabetes mellitus (GDM), the most common complication during pregnancy, highly affectsplacental function in late gestation. Advanced glycation end-products (AGEs), a complex and heterogeneous group ofcompounds engaged by the receptor for AGEs (RAGE), are closely associated with diabetes-related complications. Inthis study, AGEs induced a decrease in the expression of tight junction (TJ) proteins in BeWo cells and increased theparacellular permeability of trophoblast cells by regulating RAGE/NF-κB. Sprague-Dawley (SD) rats injected with100 mg/kg AGEs-rat serum albumin (RSA) via the tail vein from embryo day 2 were set as the placental barrierdysfunction model group (n = 10). The effect of AGEs on placental permeability was determined using the EvansBlue dye extravasation method. The ultrastructure of the placenta samples was observed by transmission electronmicroscopy. The effects of AGEs on the placenta were confirmed by treating rats with RAGE antagonist FPS-ZM1and soluble forms of RAGE (sRAGE). AGEs treatment increased placental permeability and disrupted the tightjunctions in pregnant rat placenta, but has no effect on blood glucose. The expression of TJ-related proteins,including ZO-1, Occludin, and Claudin 5, were downregulated after AGEs treatment. Further, AGEs treatmentincreased the expression of RAGE and nuclear factor-κB in the placenta of rats and upregulated the levels of vascularendothelial growth factor. The effects of AGEs on the placenta were blocked by RAGE antagonist FPS-ZM1 andsRAGE. This study demonstrates the mechanism underlying AGEs-induced disturbance in placental function inpregnant rats and highlights the potential of AGEs in the treatment of GDM. 相似文献