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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
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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
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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
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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
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Eduardo Fernandes Bondan Maria De Fátima Monteiro Martins 《Microscopy research and technique》2013,76(7):714-722
The use of cyclosporine (CsA) has shown to induce an increase in density of oligodendrocytes near remyelinating areas following the injection of ethidium bromide (EB), a demyelinating agent, in the rat brainstem. It is also known that diabetes mellitus was capable of delaying remyelination by both oligodendrocytes and Schwann cells in this gliotoxic model. This study was designed to assess whether CsA had the capacity to improve remyelination in streptozotocin‐induced (50 mg/kg, intraperitoneal route) diabetic rats. Diabetic Wistar rats were divided in different groups receiving 10 microlitres of 0.1% EB or 0.9% saline solution into the cisterna pontis and were treated or not with CsA. During 7 days and, thereafter, three times a week, 10 mg/kg/day of CsA were given by intraperitoneal route. The rats were euthanized from 7 to 31 days after EB or saline injection and brainstem sections were collected and processed for light and transmission electron microscopy studies. Results from different groups were compared by using a semi‐quantitative method developed for documenting the extent and nature of remyelination in semithin sections following gliotoxic lesions. Results showed that CsA administration to diabetic rats after EB injection stimulate both oligodendroglial and Schwann cell remyelination (mean remyelination scores of 3.15 ± 0.5 for oligodendrocytes and 1.36 ± 0.58 for Schwann cells) compared to untreated animals (2.52 ± 0.71 for oligodendrocytes and 0.73 ± 0.47 for Schwann cells, respectively). CsA given to diabetic rats was capable of reversing some of the deleterial effects of diabetes on remyelination. Microsc. Res. Tech. 76:714–722, 2013. © 2013 Wiley Periodicals, Inc. 相似文献
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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
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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
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本文用气相色谱/质谱法(GC/MS)证明了尼克刹米在人尿中的主要代谢产物为烟酰胺。方法简便,用样量少。 相似文献
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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
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采用气相色谱-质谱法检测人尿中非那雄胺三个代谢物。叔丁基甲醚提取,甲基睾酮作为内标,对尿样的游离部分和酶解后部分分别提取,采用HP-1MS柱(17m×0.2 mm i.d.×0.11mm),程序升温,质谱检测。发现一种羧酸代谢物(M1)和两种羟基代谢物(M2和M3),采用标准品对照确证了M1的结构;另外根据质谱特征阐明M2和M3的结构,总结三种代谢物的质谱裂解特点。初步分析三种代谢物的排泄规律,M1为主要代谢物,M2和M3为次要代谢物,M1的可检出时期最长,M3最短。该方法简单,快速,可靠,适合进行尿样的常规检测。 相似文献
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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
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目的分析年龄对微创型动态血糖监测(CGM)的影响,分析导致CGM监测异常的原因。方法连续选择2012年1月至12月于我院内分泌科诊治患者196例,按照年龄是否大于等于60岁分为老年组(105例)及对照组(91例)。2组患者均使用同一品牌型号微创型CGM仪监测血糖。结果 CGM监测中,老年T2DM组血糖过高频次、血糖过低频次及血糖异常总频次均显著高于对照组,差异有统计学意义。CGM监测异常报警原因分析中,老年T2DM组异常报警总频次、校准错误报警频次、断开报警频次及探头信号不在正常范围报警频次均显著高于对照组,差异有统计学意义。2组对象CGMS中图像异常原因分析中,老年T2DM组老年T2DM组图像异常总次数、关机原因次数均显著高于对照组,差异有统计学意义。结论老年T2DM患者CGM监测易出现血糖异常、异常报警及图像异常,医护人员应通过详细讲解接受CGM监测注意事项、制定老年患者CGM监测方案、规范CGM操作流程降低异常发生率。 相似文献
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Two different fluorescence stains, green: 5-hexadecanoylaminofluorescein, and red: BODIPY® 665/676 [( E,E )-3, 5-bis-(4-phenyl-1,3-butadienyl)-4,4-difluoro-4-bora-3a, 4a-diaza- s -indacene, produced good results regarding the demonstration of glycolipids, free fatty acids and triglycerides in mammalian skin material that had been embedded in a water miscible plastic resin (Technovit® 7100). In this way, functional aspects of specific structures (epidermal barrier region, sebaceous glands) could be characterized histochemically in the integument of five mammalian species with sparse or dense hair coats. 相似文献
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Divicine is an active pyrimidine aglycone, generated from vicine by the enzyme β-glucosidase upon ingestion of fava beans. In this study, we investigated the effect of divicine on cultured human umbilical vein endothelial cells (HUVECs) and explored the potential mechanisms. Incubation HUVECs with 18.5–85.1 μM divicine resulted in a concentration and time dependent decrease of cell viability, followed by decrease of cellular reduced glutathione, as well as increase of reactive oxygen species (ROS), malondialdehyde (MDA), and labile iron pool. Transmission electron microscopy confirmed that the divicine treated HUVECs’ mitochondria had shrunk. Importantly, the administration of desferrioxamine, an iron chelator, to the divicine treated HUVECs significantly reduced iron overload and cell death and decreased cellular ROS and MDA. These results demonstrated that divicine could cause damaging of endothelial cells, and ferroptosis might be involved in divicine induced HUVECs injury, reminding long term ingestion of fava beans might be harmful to vascular system, especially for those suffering from glucose 6-phosphate dehydrogenase deficiency. 相似文献
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Ciprofloxacin (CFX) is an effective and relatively safe antimicrobial used in a variety of human infections. However, adverse drug reactions and positive results in genotoxic tests are reported.
In order to understand the possible pathophysiological mechanisms of the toxic effects informed for CFX, lipid hydroperoxides (LOOH) -oxidative mediators of peroxidation- were quantified in liver and kidney of mice, after 15 to 360 minutes of the ciprofloxacin administration at doses of 10 mg/ Kg or 100 mg/ Kg by ip route. The peroxidation in the lipid fraction was evaluated by measuring the amount of hydroperoxides through the oxidation of 1- naphthyldiphenylphospine into its oxide and further quantification by high performance liquid chromatography.
The initial content of lipid hydroperoxides (nmol/g tissue) was 253 ± 3 in kidney and 143 ± 12 in liver. CFX induced the maximal variation to 728 ± 101 in kidney (P < 0.05) and 315 ± 31 in liver (P < 0.01), after 15 min of 100 mg/ Kg single dose. The variation in the LOOH levels was significant in kidney with both doses used and in liver after 100 mg/ Kg until 60 min after the CFX administration, and then gradually fell to natural levels.
The results demonstrated the effect of CFX on lipid oxidation, an indicator of oxidative effect. A natural protective capacity against this oxidation, more efficient in liver than in kidney, was observed. 相似文献
In order to understand the possible pathophysiological mechanisms of the toxic effects informed for CFX, lipid hydroperoxides (LOOH) -oxidative mediators of peroxidation- were quantified in liver and kidney of mice, after 15 to 360 minutes of the ciprofloxacin administration at doses of 10 mg/ Kg or 100 mg/ Kg by ip route. The peroxidation in the lipid fraction was evaluated by measuring the amount of hydroperoxides through the oxidation of 1- naphthyldiphenylphospine into its oxide and further quantification by high performance liquid chromatography.
The initial content of lipid hydroperoxides (nmol/g tissue) was 253 ± 3 in kidney and 143 ± 12 in liver. CFX induced the maximal variation to 728 ± 101 in kidney (P < 0.05) and 315 ± 31 in liver (P < 0.01), after 15 min of 100 mg/ Kg single dose. The variation in the LOOH levels was significant in kidney with both doses used and in liver after 100 mg/ Kg until 60 min after the CFX administration, and then gradually fell to natural levels.
The results demonstrated the effect of CFX on lipid oxidation, an indicator of oxidative effect. A natural protective capacity against this oxidation, more efficient in liver than in kidney, was observed. 相似文献
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