Background Oxidative stress has an important role in the pathogenesis of doxorubicin-induced hepatotoxicity. The aim of this study was to investigate the hepatoprotective effects of erdosteine, an ...antioxidant agent, on doxorubicin-induced hepatotoxicity. Methods Rats were divided into control, doxorubicin alone (20 mg/kg, i.p.) and doxorubicin plus erdosteine (50 mg/kg/day, oral) groups. At the end of the 10th day, liver tissues were removed for light microscopy and analysis. The levels of tissue protein carbonyl content, malondialdehyde and nitric oxide, as well as the activities of superoxide dismutase, catalase, were determined. Results The tissue of the doxorubicin group showed some histopathological changes such as necrosis, hepatocyte degeneration, sinusoidal dilatation, hemorrhage and vascular congestion and dilatation. In the doxorubicin plus erdosteine group, histopathological evidence of hepatic damage was markedly reduced. Biochemical parameters were consistent with histological parameters. Conclusions Doxorubicin caused hepatotoxicity, and erdosteine treatment prevented lipid peroxidation and protein oxidant in liver tissue.
The aim of this study was to determine the transportations of rivastigmine containing from various liposome formulations through Madin Darby Canine Kidney (MDCK) cells monolayer and to compare the in ...vitro test results with in vivo. There is no other liposome formulation of rivastigmine and the transportations of rivastigmine through MDCK cell monolayers or related study available in the literature. Cytotoxicity (MTT) test was used to determine cell viabilities. The effect of sodium-taurocholate or dimethyl-beta-cyclodextrine as penetration enhancer was also investigated. Characterization and stability studies for liposome formulations were performed. Permeation experiments of rivastigmine were performed through MDCK cells and dialysis membrane. The kinetic of release from liposomes was also investigated. The highest apparent permeability coefficient (log. values) was obtained with sodium-taurocholate liposomes for −1.15 ± 0.16 for MDCK cell. Rivastigmine liposomes and solutions were also administered to mice orally and intraperitonally. Acetylcholinesterase (AChE) activity was determined by Ellman method. AChE% inhibition values were calculated for both blood and brain after administration of rivastigmine solution and liposomes. The highest AChE inhibition was observed for rivastigmine-sodium-taurocholate liposomes. Histological observations of the mice' brains were performed under transmission electron microscope (TEM). The histological results were also indicated and supported all these findings.
Our first aim was to determine the total leukocyte profile in implantation. Second aim was to detect the changes in uterine leukocyte profile in diabetes, a common accompanying disease. For this ...purpose 4 groups are formed with Wistar albino rats weighing 250-300 g. Two of the groups were non-diabetic and two of them were diabetic. One of the diabetic and one of the non-diabetic groups were left pregnant. Then uterus tissues of pregnant animals were removed in the 5th and 7th days of pregnancy together with tissues of other two non-pregnant groups. Tissues were analyzed immunohistochemically with antibodies CD45, CD3, CD4, CD8, CD56, CD68 and CD79a. It was revealed that pregnancy increased immune staining of CD68, CD3, CD45 and CD56 in endometrium. In addition it was observed that immune staining density of CD68, CD45 and CD56 decreased in diabetes. In the histopathological examination, significant degeneration was detected in the endometrium of diabetic rats. Diabetes could decrease leukocyte proportions in decidua in early pregnancy periods. Therefore immune cell therapies could be administrated in diabetes related problems of pregnancy.
Objectives. Cyclosporine A (CsA) is used for the treatment of autoimmune and inflammatory disorders. However, CsA-induced nephrotoxicity remains an important clinical problem, and oxidative stress ...has been implicated as a possible responsible mechanism. We assessed the protective ability of N-acetylcysteine (NAC), an antioxidant, against CsA-induced nephrotoxicity. Materials and Methods. Wistar albino rats were randomly assigned into four groups. Group 1 rats were treated with sodium chloride as control, group 2 with CsA, group 3 with CsA and NAC, and group 4 with NAC alone. Animals were sacrificed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), malondialdehyde (MDA) and nitric oxide (NO) levels, and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities. Kidney sections were analyzed for MDA and NO levels and SOD and GSH-Px activities, as well as histopathological changes. Results. Overall, the treatment of rats with CsA alone produced significant increases in NO and MDA levels and significant decreases in SOD and GSH-Px activities in serum and renal samples. Morphological changes, including tubular epithelial atrophy, vacuolizations, and cellular desquamations, were clearly observed in the rats treated with CsA alone. Concurrent NAC administration with CsA improved renal function, as indicated by lower BUN and Cr values. Moreover, NAC significantly reduced MAD and NO levels and increased SOD and GSH-Px activities in serum and renal tissue, as well as provided a histologically proven protection against CsA-induced nephrotoxicity. Conclusion. These results indicate that NAC produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role for oxidative stress in pathogenesis.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
Abstract Background: NSAIDs have been found to induce gastrointestinal tract damage. Recently, it has been suggested that this might be mediated by lipid peroxidation. Objective: The aim of this ...study was to assess the potential protective effects of β-glucan against acetylsalicylic acid (ASA-induced gastric damage by means of its antioxidant capacity in an experimental rat model. Methods: Thirty-two male Wistar albino rats (200–250 g) were randomized into 4 groups consisting of 8 rats each. The β-glucan group received 50 mg/kg β-glucan once a day for 10 days and 30 minutes before anesthesia. The ASA group received saline once a day for 10 days and 300 mg/kg (20 mg/mL) ASA as a single dose, 4 hours before anesthesia. The ASA+β-glucan group was administered 50 mg/kg β-glucan once a day for 10 days and 30 minutes before anesthesia. Additionally, 300 mg/kg (20 mg/mL) ASA was administered as a single dose, 4 hours before anesthesia. The control group received saline once a day for 10 days and 30 minutes before anesthesia. All medications were administered by intragastric gavage. The stomach from each rat was dissected and divided into 2 parts for histologic and biochemical analysis. Gastric tissue malondialdehyde (MDA), nitric oxide (NO) levels, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities were determined for oxidative parameter analysis. Results: The gastroprotective and antioxidant effects of β-glucan appeared to attenuate the ASA-induced gastric tissue damage. Compared with the control group, MDA and NO levels and CAT and GSH-Px activities were significantly increased in the stomachs of ASA-treated rats (MDA, 4.12 0.44 to 13.41 1.05 μmol/L; NO, 8.04 7.25–9.10 vs 30.35 22.34–37.95 μmol/g protein; CAT, 0.050 0.004 to 0.083 0.003 k/g protein; GSH-Px, 0.57 0.42–0.66 to 1.55 1.19–1.76 U/L; all, P < 0.001), whereas SOD activity was significantly decreased in the same group (291 29 to 124 6 U/mL; P < 0.001). In the ASA+β-glucan group, MDA and NO levels and CAT and GSH-Px activities were found to be significantly lower, while SOD activity was found to be significantly higher, in comparison with the ASA-treated group (all, P < 0.001). Conclusion: β-Glucan appeared to attenuate the gastric damage caused by ASA in these rats.
Caffeic acid phenethyl ester (CAPE) is a natural product with potent anti-inflammatory, antitumor and antioxidant activities and attenuates inflammation and lipid peroxidation induced by ...ischemia-reperfusion injury. The purpose of the present study was to investigate the effects of CAPE on isoproterenol (ISO) -induced myocardial infarction.
A randomized controlled experimental design was used in this study. Rats were divided into four groups and treated with saline, CAPE, ISO and ISO+CAPE. Rats were treated with CAPE (10 micromol kg/day i.p.) or saline starting 3 days before injecting ISO (150 mg /kg s.c., 24 hours). Seven days later, rats were sacrificed and the hearts were excised for biochemical analyses and microscopic examination. One-way ANOVA test with post hoc multiple comparisons using LSD method were used for statistical analysis of the data.
The administration of ISO alone resulted in higher myeloperoxidase (MPO) activity, lipid peroxidation, superoxide dismutase (SOD) and catalase (CAT) than in the control. The enzyme activities did not change in rat given CAPE alone. CAPE treatment prevented the increase in MPO activity and malondialdehyde, but did not affect the activities SOD and CAT enzymes.
In light of these results, we conclude that CAPE prevents MPO-and lipid peroxidation-mediated myocardial injury via inhibition of neutrophil's MPO activity.
Alport Syndrome (AS) is an important hereditary disorder affecting the glomerular basement membrane. Diagnosis of AS is based on the presence of hematuric nephropathy, renal failure, hearing loss, ...ocular abnormalities and changes in the glomerular basement membrane of the lamina densa. The aims of this case report were to show the changes in the gingival tissues in a patient with AS under therapy with cyclosporin-A after renal transplantation and to discuss the possible role of type IV collagen in gingival basal lamina as an alternative approach for the diagnosis of AS. A 20-year-old male patient with AS underwent periodontal therapy including a series of gingivectomy surgeries. Gingival samples obtained during the second surgery were examined histopathologically and by transmission electron microscopy for further pathological examination. Gingivectomy procedures have been performed every 6 months over the last 4 years. The excessive and fibrous gingival enlargements resulted in migration of the anterior teeth, but no alveolar bone loss occurred. This is the first report to demonstrate the possible changes in the gingival tissues caused by AS. It is suggested that gingival biopsy can be an initial diagnostic tool instead of renal or skin biopsies. Proper dental and periodontal care and regular visits to the dentist could provide limited gingival hyperplasia to patients with AS.
Summary Metabolic and immune systems are very important for a living organism to survive. Since they play crucial roles in maintaining homeostasis, both systems work interdependently. In metabolic ...disorders like obesity and related diseases, lot of reports have been published about immune system impairment. In addition, in the case of malnutrition and calorie restriction, immune system is affected through several mechanisms. Different from the current point of view, I propose an unusual way of thinking about the relationship between immune and metabolic systems. The nutrient-based ecosystemic balance; the simple desires and rules like feeding or reproduction underlying very complex relations among species; the beneficial effects of caloric restriction; and the similarities between the pathways contributing obesity and infection made me look from a different perspective. Based on ecology and systems thinking, the present hypotheses suggest that pathologic organisms could be a kind of dietary source for lymphoid cells. If it is true, it will bring new and hopeful insights to all events related to metabolic and immune systems. At first, new mechanisms could be improved to defeat unbeatable organisms like Mycobacterium tuberculosis or HIV. The unphagocytosed organisms could be unknown tastes for our body’s defenders. For example, the lymphoid cells could be classified as virovores, bacterivores, or fungivores like herbivores, and carnivores. Secondly, this basic relation could be used to solve huge problems caused by obesity related disorders like diabetes, because insulin would play more important roles for lymphoid cells while regulating the blood glucose level if the hypothesis is true. And the persistence of hyperglycemia would mainly effect lymphoid cells according to the current hypothesis.
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