The safety of food additives E407 and E407a has raised concerns in the scientific community. Thus, this study aims to assess the local and systemic toxic effects of the common food additive E407a in rats orally exposed to it for two weeks. Complex evaluations of the effects of semi-refined carrageenan (E407a) on rats upon oral exposure were performed. Local effects of E407a on the intestine were analyzed using routine histological stains and CD68 immunostaining. Furthermore, circulating levels of inflammatory markers were assessed. A fluorescent probe O1O (2- (2′-OH-phenyl)-5-phenyl-1,3-oxazole) was used for evaluating the state of leukocyte cell membranes. Cell death modes of leukocytes were analyzed by flow cytometry using Annexin V and 7-aminoactinomycin D staining. Oral administration of the common food additive E407a was found to be associated with altered small and large intestinal morphology, infiltration of the lamina propria in the small intestine with macrophages (CD68+ cells), high systemic levels of inflammation markers, and changes in the lipid order of the phospholipid bilayer in the cell membranes of leukocytes, alongside the activation of their apoptosis. Our findings suggest that oral exposure to E407a through rats results in the development of intestinal inflammation.
Gadolinium orthovanadate GdVO4:Eu3+ nanoparticles (VNPs) have been shown to scavenge reactive oxygen species (ROS), making them a promising therapeutic agent in inflammation.This study aims to assess the effects of VNPs administered orally on E407a-induced inflammation.Materials and Methods: Fragments of the small intestine of 8 rats treated orally with a carrageenan-containing food additive E407a at a dose of 140 mg / kg of weight during 2 weeks, 8 animals orally exposed to both E407a and VNPs at a dose of 20 µg / kg of weight during the same period of time, and 8 control rats were stained routinely and immunostained for CD3 and CD68 with the subsequent immunohistochemical scoring. Moreover, analysis of viability and cell death modes of granulocytes was performed by flow cytometry using Annexin V and 7aminoactinomycin D (7-AAD).Results: Oral exposure to the food additive E407a resulted in the development of enteritis associated with altered small intestinal morphology, infiltration of the lamina propria with macrophages and T-lymphocytes, and activation of peripheral blood granulocyte apoptosis. VNPs administered against the background of E407a-induced slight intestinal inflammation improved small intestinal morphology, decreased infiltration rate of the immune cells mentioned above without affecting the intensity of granulocyte apoptosis. Conclusion:Oral administration of VNPs ameliorates E407a-induced enteritis.
Aim: To evaluate the effects of orally administered gadolinium orthovanadate GdVO4:Eu3+ nanoparticles (VNPs) on the course of chronic carrageenan-induced intestinal inflammation. Methods: Samples of small intestinal tissue were collected from four groups of rats (intact, after administration of VNPs, with carrageenaninduced intestinal inflammation, with carrageenan-induced intestinal inflammation orally exposed to VNPs) to assess the intestinal morphology and HSP90α expression. Levels of seromucoid, C-reactive protein, TNF-α, IL-1β and IL-10 were determined in blood serum. Results: Oral exposure to VNPs was associated with neither elevation of inflammation markers in blood serum nor HSP90α overexpression in the small intestine, i.e. no toxic effects of VNPs were observed. Carrageenan-induced intestinal inflammation was accompanied by higher levels of TNF-α and IL-1β, as well as HSP90α upregulation in the intestinal mucosa, compared with controls. Administration of VNPs to rats with enteritis did not lead to statistically significant changes in concentrations of circulating pro-inflammatory cytokines with the trend towards their increase. Conclusion: No adverse effects were observed in rats orally exposed to VNPs at a dose of 20 μg/kg during two weeks. Using the experimental model of carrageenan-induced enteritis, it was demonstrated that VNPs at the dose used in our study did not affect the course of intestinal inflammation.
Objective. The aim of this study was to assess the vascular endothelium morphofunctional state of the brain microcirculatory bed in rats with nitrite-induced Alzheimer's type dementia on the background of stem cells administration. Methods. 14 days after the experiment's end, the endothelin-1, VEGF-A, eNOS, von Willebrand factor were determined in blood serum by the enzyme immunoassay and photometric methods in rats with a model of nitrite-induced dementia (14 and 28 days of sodium nitrite intraperitoneal introduction) with and without mesenchymal stem cells (MSCs) administration. The brain slices were stained according to the Einarson's method and immunohistochemically by staging the reaction with antibodies to VEGF. Results. With an increase in the sodium nitrite administration period, the degree of damage of brain capillaries and neurons increased, dystrophy of "surviving" neurons developed and ability to produce VEGF decreased. After 14 days of "regeneration period" in groups without MSCs administration, further stimulation of VEGF production by endotheliocytes, cortex and hippocampus neurons of varying degrees was observed. In groups where stem cells were introduced, the number of capillaries increased, with endothelial hyperplasia in some cases. Conclusion. In animals with nitrite-induced dementia, dose-dependent damage to the endothelium of the capillary bed is noted. From the first day damage the vascular regeneration can be proved by VEGF expression. The stem cells administration more effectively stimulates capillary regeneration, as evidenced by a noticeable increase of the number of brain capillaries.
Objective. The aim of the study was to evaluate vimentin expression in inflamed nasal mucosa of patients with chronic rhinosinusitis without nasal polyps (CRSsNP) and serum levels of matrix metalloproteinase-9 (MMP-9). Material and Methods. We measured concentrations of MMP-9 in blood serum of twenty patients with CRSsNP using ELISA and compared them with the control group composed of twenty healthy subjects. Vimentin expression in nasal mucosa was studied by an immunohistochemical method. Results. Blood serum levels of MMP-9 were found to be elevated in patients with CRSsNP. The disease was also associated with the upregulation of vimentin expression both in the lamina propria and nasal epithelial layer. Conclusion. CRSsNP is accompanied by a higher number of vimentin-expressing cells in the nasal epithelium, which may indicate their epithelial-to-mesenchymal transition (EMT). We speculate that MMP-9 may contribute to the increased rate of EMT of nasal epithelial cells in CRSsNP.
Харківський національний медичний університет, Україна Стаття присвячена вивченню особливостей постнатального морфогенезу ацинарної тканини привушної слинної залози тримісячних щурів, які народилися з експериментально модельованою макросомією в різних варіаціях. Мета роботи-вивчення в експерименті особливостей постнатального морфогенезу слинних залоз тримісячних щурів, які народилися макросомами. Матеріали та методи. Аналізували соматометричні показники тварин на момент народження та при виведенні з експерименту, в якому моделювали макросомію плода 4 способами (висококалорійна дієта молодих вагітних самиць, висококалорійна дієта вагітних самиць зрілого віку, висококалорійна дієта та гіпокінезія молодих вагітних самиць, посилене плацентарно-плодове кровопостачання на тлі звичайних умов існування молодих вагітних самиць). Для морфологічного аналізу використовували тканини привушних слинних залоз тримісячних щурів-нащадків. Оцінювали абсолютні та відносні значення маси слинних залоз. Крім гістологічного аналізу для виявлення ДНК і РНК використали забарвлення галоціанін-хромовими галунами за Ейнарсоном, для виявлення глікопротеїдів поставили PAS-реакцію. Використовуючи комп'ютерні зображення, виміряли площу ядер сероцитів, оцінили вміст ДНК в ядрі, РНК у цитоплазмі, глікопротеїдів у слині протоків і просвітів ацинусів. Результати. При досягненні щурами-нащадками тримісячного віку в макросомів зі стимульованим внутрішньоутробним ростом (група Акс) середня маса тіла має тенденцію до збільшення, а в макросомів-нащадків батьків молодого віку, вагітність матерів яких відбувалась в умовах «м'якої» гіпокінезії та надмірної калорійності харчування (група М+Гк+cal),-до зменшення. У макросомів-нащадків молодих батьків, які під час вагітності споживали їжу підвищеної калорійності (група М+cal), та в макросомів-нащадків батьків зрілого віку, котрі під час вагітності одержували гіперкалорійну дієту (група З+cal), соматометричні показники були аналогічні контролю. Відносна маса привушних слинних залоз у тримісячних щурів, які народились із макросомією, виявилася збільшеною в усіх варіантах моделювання, але максимально у групах М+cal та М+Гк+cal. У макросомів групи Акс у тримісячному віці формуються слинні залози з гіпоплазією сероцитів, що морфофункціонально активніші, з ознаками гіперпродукції білків і гіпопродукції глікопротеїдів. У макросомів групи М+cal у тримісячному віці кінцеві відділи слинної залози сформовані аналогічно контролю за кількістю сероцитів, але сероцити морфофункціонально активніші, з ознаками гіперпродукції глікопротеїдів. У макросомів групи З+cal у тримісячному віці спостерігається гіперплазія сероцитів, морфофункціональний стан яких не відрізняється від такого в контрольних тварин. У макросомів групи М+Гк+cal спостерігають ознаки збільшення морфофункціональної активності сероцитів із гіперпродукцією глікопротеїдів. Висновки. В особин, які народились із макросомією, у тримісячному віці спостерігається зміна морфофункціонального стану паренхіми привушних слинних залоз і складу слини у протоках, просвітах ацин...
The article shows the features of the pathomorphosis of gunshot bullet wounds to the abdomen with damage to the colon. Various options for the course of repair and regeneration of the colon after surgical treatment and in the presence of postoperative complications in wounded patients with and without concomitant pathology of the colon are provided. It is shown that the etiology and pathogenesis of a penetrating gunshot wound of the intestine has mechanical and metabolic aspects. It has been proven that the greatest impact force on the intestine falls on the outside, on the peritoneum, which is often worn away from the longitudinal layer of the muscle wall of the intestine. It is given that the restructuring of the structure and function of the colon in chronic colitis after a gunshot wound leads to an exacerbation of the chronic process in all membranes. It is shown that damage to the intestinal mucosa occurs simultaneously with the destruction of intestinal tissues, but depends on general and local immunity. Infiltration of the site of the lesion by neutrophil granulocytes leads to the disposal of the entire wound or the development of complications. The structural and functional state of intestinal lymphatic follicles makes it possible to maintain intestinal immune protection, bacterial microflora and digestion. The method of choice for surgical repair of the consequences penetrating into the abdominal cavity of a gunshot wound will be the maximum resection of necrotic foci, large hemorrhages to avoid adhesion disease. At different levels, depending on the wound process, the structural and functional reconstruction is completely different, which is due to the individual feature of the structure and function, which affects the surgeon's desire for a justified radical or, on the contrary, for an organ-preserving operation. Keywords: histological examination, gunshot wound, colon injury.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.