СУБМІКРОСКОПІЧНІ ЗМІНИ КОМПОНЕНТІВ АЕРОГЕМАТИЧНОГО БАР’ЄРУ РЕСПІРАТОРНОГО ВІДДІЛУ ЛЕГЕНЬ ЩУРІВ У РАННІ ТЕРМІНИ ПІСЛЯ ГОСТРОГО УРАЖЕННЯ ХЛОРИДНОЮ КИСЛОТОЮ

Submicroscopic studies of the respiratory part of the lungs after 2 and 6 hours after the experimental acute lung injury with hydrochloric acid established adaptive-compensatory and destructive changes in the components of the air-blood barrier.The aim of the study – to learn submicroscopic changes in the components of the air-blood barrier of the lungs in the early period after acute lung injury.Materials and Methods. The experiments were carried out on 30 white mature non-linear male rats weighing 200–220 g. The animals were divided into 3 groups: 1 – control group, 2 – hydrochloric acid damage after 2 hours, 3 – hydrochloric acid damage after 6 hour.Results and Discussion. In an experiment on mature white rats, a study was made of the submicroscopic state of the components of the air-blood barrier in the early periods after acute lung injury. It has been established that adaptive-compensatory and initial destructive changes of the alveolar epithelium and the walls of the hemocapillary take place at 2 o'clock in the experiment. The cytoplasm of respiratory epitheliocytes during this period of the experiment was focal-edematous and enlightened, organelles were destructively altered. For alveolocytes of type I, there was a significant swelling and clarification of the cytoplasm. During this period of the experiment, an increased number of actively phagocytizing macrophages appeared, which acquired a rounded shape, clearly contoured membranes of the cariolema, their invaginations were determined, and in the karyoplasm euchromatin predominated. In alveolocytes of type II, after 6 hours, the progression of destructive changes was established. For which there were peculiarity hypertrophied nuclei with deep invagination of the cariolema, in which there were few nuclear pores, locally expanded perinuclear space. In the edematous cytoplasm, organelles were found to be destructively altered.Conclusions. Acute damage to the lungs leads to a disruption of the ultrastructural organization of the air-blood barrier. Established adaptive-compensatory processes and signs of destructive changes in the alveolar epithelium and the walls of hemocapillaries, which leads to deterioration of gas-exchange processes in the lungs.

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Colloidal gold particles as a new in vivo marker of early acute lung injury

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00078.2004 ◽

2004 ◽

Vol 287 (4) ◽

pp. L867-L878 ◽

Cited By ~ 53

Author(s):

Kai Heckel ◽

Rainer Kiefmann ◽

Martina Dörger ◽

Mechthild Stoeckelhuber ◽

Alwin E. Goetz

Keyword(s):

Electron Microscopy ◽

Acute Lung Injury ◽

Gas Exchange ◽

Lung Injury ◽

Colloidal Gold ◽

Microvascular Permeability ◽

Arterial Oxygen ◽

Control Group ◽

Gold Particles

Permeability of the endothelial barrier to large molecules plays a pivotal role in the manifestation of early acute lung injury. We present a novel and sensitive technique that brings microanatomical visualization and quantification of microvascular permeability in line. White New Zealand rabbits were anesthetized and ventilated mechanically. Rabbit serum albumin (RSA) was labeled with colloidal gold particles. We quantified macromolecular leakage of gold-labeled RSA and thickening of the gas exchange distance by electron microscopy, taking into account morphology of microvessels. The control group receiving a saline solution represented a normal gas exchange barrier without extravasation of gold-labeled albumin. Infusion of lipopolysaccharide (LPS) resulted in a significant displacement of gold-labeled albumin into pulmonary cells, the lung interstitium, and even the alveolar space. Correspondingly, intravital fluorescence microscopy and digital image analysis indicated thickening of width of alveolar septa. The findings were accompanied by a deterioration of alveolo-arterial oxygen difference, whereas wet/dry ratio and albumin concentration in the bronchoalveolar lavage fluid failed to detect that early stage of pulmonary edema. Inhibition of the nuclear enzyme poly(ADP-ribose) synthetase by 3-aminobenzamide prevented LPS-induced microvascular injury. To summarize: colloidal gold particles visualized by standard electron microscopy are a new and very sensitive in vivo marker of microvascular permeability in early acute lung injury. This technique enabling detailed microanatomical and quantitative pathophysiological characterization of edema formation can form the basis for evaluating novel treatment strategies against acute lung injury.

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Protection Effectiveness Of Bit (Beta vulgaris) Fruit Extract In Maintaining Spermatogenesis Ability In White Rats (Rattus novergicus) Induced Carbon Tetracloride (CCl4)

Journal of Basic Medical Veterinary ◽

10.20473/jbmv.v10i2.31812 ◽

2021 ◽

Vol 10 (2) ◽

pp. 36

Author(s):

Alvyan Lantang Anugrah ◽

Hana Eliyani ◽

Budi Utomo ◽

Suherni Susilowati ◽

Maslichah Mafruchati ◽

...

Keyword(s):

Beta Vulgaris ◽

Sertoli Cells ◽

Negative Control Group ◽

Positive Control ◽

Negative Control ◽

Male Rats ◽

Control Group ◽

Root Extract ◽

Beet Root ◽

White Rats

The aim of this research was to know whether beetroot (Beta Vulgaris) extract could protect spermatogenesis by maintaining spermatogenic and sertoli cell count in rats (Rattus novergicus) induced with CCl4. Rats were given beetroot extract daily, for 14 days and 3ml/kg BW CCl4 intraperitoneally one hour after last treatment. This study used twenty rats which were devided equally into 5 groups. K(-), the negative control group was not induced with CCL4 and only given 1% CMC-Na suspension. K(+), the positive control group was induced with CCl4 and given 1% CMC-Na suspension. P1, P2 and P3 were given beet root extract with doses of 200, 400, and 800 mg/kg BW daily before feeding. All of the beetroot treatment were given orally (2 ml). After 24 hours CCl4 induction, rats were sacrificed and testis were collected to make histology slides. The observations showed significantly different (p<0,05) in all of variables. Result showed significant differences in spermatogenic and sertoli cells between K(-) and K(+) groups, K(+) with P2 and P3 group, and showed insignificant difference between P2 and P3 group in spermatogenic and sertoli cells. The result of this research showed that beetroot extract could protect the spermatogenic and sertoli cells in male rats induced with CCl4.

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Alveolar epithelium and Na,K-ATPase in acute lung injury

Intensive Care Medicine ◽

10.1007/s00134-007-0661-8 ◽

2007 ◽

Vol 33 (7) ◽

pp. 1243-1251 ◽

Cited By ~ 69

Author(s):

István Vadász ◽

Stacy Raviv ◽

Jacob I. Sznajder

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Alveolar Epithelium

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TOTAL FLAVONOID DAN EFEKTIVITAS EKSTRAK ETANOL BIJI KELOR (Moringa oleifera L) ASAL KOTA PALU SULAWESI TENGAH TERHADAP HISTOPATOLOGI PANKREAS TIKUS PUTIH JANTAN (Rattus norvegicus) YANG DIINDUKSI STREPTOZOTOCIN

Jurnal Ilmiah Manuntung ◽

10.51352/jim.v6i1.294 ◽

2020 ◽

Vol 6 (1) ◽

pp. 24

Author(s):

Viani Anggi ◽

Joni Tandi ◽

Veronika Veronika

Keyword(s):

Ethanol Extract ◽

Negative Control ◽

Total Flavonoid ◽

Male Rats ◽

Control Group ◽

Β Cells ◽

Pancreatic Β Cells ◽

White Rats ◽

Group I ◽

Streptozotocin Induced Diabetes

This study aims to determine the content of flavonoid and the effect of ethanol extract of moringa seeds on the regeneration of pancreatic β cells in male white rats streptozotocin induced diabetes. This study method used has total flavonoid equivalent quercetin by spectrophotometry uv-vis and to regeneration of pancreatic β cells in male white rats used 30 test animals,namely male white rats divided into 6 groups, each group consisted of 5 male white rats with details of group I as normal control, Group II as negative control given 0.5% Na-CMC suspension, Group III as positive control given glibenclamide suspension and in Groups IV, V, and VI were given with each dose of 100 mg/kg BW, 200 mg/kg BW and 400 mg/kg BB. Histopathological damage picture of the pancreas was observed by staining HE using a 400x magnification olympus Cx21 microscope. The results showed that the ethanol extract of moringa seeds contained secondary metabolites, namely flavonoids, alkaloids, saponins and tannins. The results showed has total flavonoid equivalent quercetin of moringa seeds is 1,26% and regeneration of pancreatic β cells in male white rats streptozotocin induced diabetes of Moringa seed ethanol extract at a dose of 400 mg/kg BB can have an effect on the regeneration of β cells in the pancreas of white diabetic male rats.

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Acute lung injury inhibition by juglone in LPS induced sepsis mouse model involves Sirt1 activation

Tropical Journal of Pharmaceutical Research ◽

10.4314/tjpr.v19i5.14 ◽

2020 ◽

Vol 19 (5) ◽

pp. 1001-1007

Author(s):

Qiong Hu ◽

Chunai Yang ◽

Fenshuang Zheng ◽

Hongdan Duan ◽

Yangshan Fu ◽

...

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Mouse Model ◽

Inflammatory Cytokines ◽

Alveolar Epithelial Cells ◽

Control Group ◽

Western Blot Assay ◽

Edema Formation ◽

Sirt1 Expression ◽

Treatment Groups

Purpose: To investigate the effect of juglone on LPS induced lung injury in a mouse model and in TC 1cell line.Methods: Edema formation in lungs were measured by determination of lung wet/dry weight. Expressions of various proteins were assessed by western blot assay, while Sirt1 level was assessed using immunohistochemistry. Mice were randomly assigned to nine groups of 10 mice each: normal control, untreated and seven juglone treatment groups. Acute lung injury was induced in mice by injecting LPS (10 mg/kg) via intraperitoneal route (ip). The treatment groups were given 10, 20, 30, 40, 50, 60 and 100 μM of juglone, ip, respectively.Results: The levels of MMP-9, IL-6, IL-1β and iNOS were significantly higher in acute lung injury induced mice compared than the control group (p < 0.05). Treatment of the mice with juglone significantly decreased LPS-induced up-regulation of inflammatory cytokines in a dose-dependentmanner. The production of inflammatory cytokines was almost completely inhibited in the mice treated with 100 mg/kg dose of juglone, while treatment of the LPS-stimulated TC 1 cells with juglone upregulated the expression of Sirt1 mRNA. Down-regulation of Sirt1 expression by siRNA inhibited the effect of juglone on LPS-induced increase in inflammatory cytokine production.Conclusion: Juglone prevents lung injury in mice via up-regulation of Sirt1 expression. Therefore, juglone might be useful for the development of a treatment strategy for lung injury. Keywords: Inflammatory, Sirtuin, Edema, Cytokines, Lung injury, TC 1 lung alveolar epithelial cells, Sirt1

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Animal models of acute lung injury

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00010.2008 ◽

2008 ◽

Vol 295 (3) ◽

pp. L379-L399 ◽

Cited By ~ 845

Author(s):

Gustavo Matute-Bello ◽

Charles W. Frevert ◽

Thomas R. Martin

Keyword(s):

Risk Factors ◽

Acute Lung Injury ◽

Animal Models ◽

Lung Injury ◽

Animal Studies ◽

Ischemia Reperfusion ◽

Alveolar Epithelium ◽

Acid Aspiration ◽

Advantages And Disadvantages ◽

Clinical Risks

Acute lung injury in humans is characterized histopathologically by neutrophilic alveolitis, injury of the alveolar epithelium and endothelium, hyaline membrane formation, and microvascular thrombi. Different animal models of experimental lung injury have been used to investigate mechanisms of lung injury. Most are based on reproducing in animals known risk factors for ARDS, such as sepsis, lipid embolism secondary to bone fracture, acid aspiration, ischemia-reperfusion of pulmonary or distal vascular beds, and other clinical risks. However, none of these models fully reproduces the features of human lung injury. The goal of this review is to summarize the strengths and weaknesses of existing models of lung injury. We review the specific features of human ARDS that should be modeled in experimental lung injury and then discuss specific characteristics of animal species that may affect the pulmonary host response to noxious stimuli. We emphasize those models of lung injury that are based on reproducing risk factors for human ARDS in animals and discuss the advantages and disadvantages of each model and the extent to which each model reproduces human ARDS. The present review will help guide investigators in the design and interpretation of animal studies of acute lung injury.

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Losartan attenuates paraquat-induced pulmonary fibrosis in rats

Human & Experimental Toxicology ◽

10.1177/0960327114543840 ◽

2014 ◽

Vol 34 (5) ◽

pp. 497-505 ◽

Cited By ~ 11

Author(s):

F Guo ◽

YB Sun ◽

L Su ◽

S Li ◽

ZF Liu ◽

...

Keyword(s):

Pulmonary Fibrosis ◽

Lung Injury ◽

Mrna Expression ◽

Collagen Type ◽

Collagen Type I ◽

Control Group ◽

Type I ◽

Expression Levels ◽

Relative Expression ◽

Tgf Β1

Paraquat (PQ) is one of the most widely used herbicides in the world and can cause pulmonary fibrosis in the cases with intoxication. Losartan, an angiotensin II type 1 receptor antagonist, has beneficial effects on the treatment of fibrosis. The aim of this study was to examine the effect of losartan on pulmonary fibrosis in PQ-intoxicated rats. Adult male Sprague Dawley rats ( n = 32, 180–220 g) were randomly assigned to four groups: (i) control group; (ii) PQ group; (iii) PQ + losartan 7d group; and (iv) PQ + losartan 14d group. Losartan treatment (intragastrically (i.g.), 10 mg/kg) was performed for 7 and 14 days after a single i.g. dose of 40 mg/kg PQ. All rats were killed on the 16th day, and hematoxylin–eosin and Masson’s trichrome staining were used to examine lung injury and fibrosis. The levels of hydroxyproline and transforming growth factor β1 (TGF-β1), matrix metallopeptidase 9 (Mmp9), and tissue inhibitor of metalloproteinase 1 (TIMP-1) messenger RNA (mRNA) expression and relative expression levels of collagen type I and III were also detected. PQ caused a significant increase in hydroxyproline content, mRNA expression of TGF-β1, Mmp9, and TIMP-1, and relative expression levels of collagen type I and III ( p < 0.05), while losartan significantly decreased the amount of hydroxyproline and downregulated TGF-β1, Mmp9, and TIMP-1 mRNA and collagen type I and III expressions ( p < 0.05). Histological examination of PQ-treated rats showed lung injury and widespread inflammatory cell infiltration in the alveolar space and pulmonary fibrosis, while losartan could markedly reduce such damage and prevent pulmonary fibrosis. The results of this study indicated that losartan could reduce lung damage and prevent pulmonary fibrosis induced by PQ.

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Role of matrix metalloprotease-9 in hyperoxic injury in developing lung

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00441.2007 ◽

2008 ◽

Vol 295 (4) ◽

pp. L584-L592 ◽

Cited By ~ 45

Author(s):

Anne Chetty ◽

Gong-Jie Cao ◽

Mariano Severgnini ◽

Amy Simon ◽

Rod Warburton ◽

...

Keyword(s):

Lung Injury ◽

Structural Changes ◽

Type I Collagen ◽

Alveolar Epithelium ◽

Mouse Lung ◽

Type I ◽

Matrix Metalloprotease ◽

Oxidant Injury ◽

Hyperoxia Exposure

Matrix metalloprotease-9 (MMP-9) is increased in lung injury following hyperoxia exposure in neonatal mice, in association with impaired alveolar development. We studied the role of MMP-9 in the mechanism of hyperoxia-induced functional and histological changes in neonatal mouse lung. Reduced alveolarization with remodeling of ECM is a major morbidity component of oxidant injury in developing lung. MMP-9 mediates oxidant injury in developing lung causing altered lung remodeling. Five-day-old neonatal wild-type (WT) and MMP-9 (−/−) mice were exposed to hyperoxia for 8 days. The lungs were inflation fixed, and sections were examined for morphometry. The mean linear intercept and alveolar counts were evaluated. Immunohistochemistry for MMP-9 and elastin was performed. MMP-2, MMP-9, type I collagen, and tropoelastin were measured by Western blot analysis. Lung quasistatic compliance was studied in anaesthetized mice. MMP-2 and MMP-9 were significantly increased in lungs of WT mice exposed to hyperoxia compared with controls. Immunohistochemistry showed an increase in MMP-9 in mesenchyme and alveolar epithelium of hyperoxic lungs. The lungs of hyperoxia-exposed WT mice had less gas exchange surface area and were less compliant compared with room air-exposed WT and hyperoxia-exposed MMP-9 (−/−) mice. Type I collagen and tropoelastin were increased in hyperoxia-exposed WT with aberrant elastin staining. These changes were ameliorated in hyperoxia-exposed MMP-9 (−/−) mice. MMP-9 plays an important role in the structural changes consequent to oxygen-induced lung injury. Blocking MMP-9 activity may lead to novel therapeutic approaches in preventing bronchopulmonary dysplasia.

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Sulfation pathway of thyroid hormone metabolism in selenium-deficient male rats

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1995.268.4.e572 ◽

1995 ◽

Vol 268 (4) ◽

pp. E572-E579

Author(s):

S. Y. Wu ◽

W. S. Huang ◽

I. J. Chopra ◽

M. Jordan ◽

D. Alvarez ◽

...

Keyword(s):

Production Rate ◽

Elevated Serum ◽

Selenium Deficiency ◽

Male Rats ◽

Tissue Type ◽

Constant Infusion ◽

Control Group ◽

Type I ◽

Metabolic Clearance ◽

Serum Concentrations

Male Sprague-Dawley rats were fed a selenium-deficient yeast-based laboratory diet or a control diet for 6 wk. The tissue type I 5'-monodeiodinase (5'-MDI) activity and the immunoassayable 5'-MDI were significantly (P < 0.05) reduced in the liver and the kidney but not in the thyroid of selenium-deficient rats. The mean serum concentrations of thyroxine sulfate (T4S), 3,3',5'-triiodothyronine sulfate (T3S), and reverse T3 sulfate (rT3S) (ng/dl) were significantly increased in selenium-deficient rats (15.7, 59.4, and 22.8, respectively, n = 12) compared with control rats (< 1.0, 18.5, and 9.1, respectively, n = 12, P < 0.01). Kinetic studies were carried out during a constant infusion of unlabeled sulfated iodothyronines (T4S, T3S, or rT3S, n = 5-6/group) at a rate of 1 microgram/h by Alzet minipump for 48 h. The data showed that elevated serum concentrations of T4S or T3S in the selenium-deficient rat are due both to reduced metabolic clearance rate (MCR, mean, l.kg-1.day-1, 7.4 for T4S and 4.5 for T3S in selenium deficiency vs. 12 and 9.2, respectively in controls, P < 0.05) and increased production rate (mean, microgram.kg-1.day-1, 1.2 for T4S, and 2.7 for T3S in selenium deficiency vs. 0.12 and 1.7, respectively, in the controls, P < 0.05). However, the increased serum rT3S concentration in selenium-deficient rats is due mainly to reduced MCR (mean, l.kg-1.day-1, 34 vs. 67 in controls, P < 0.05) and its daily production rate remained unchanged in selenium deficiency (mean, microgram.kg-1.day-1, 7.6 vs. 6.1 in the control group, P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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