Fish Oil - Omega-3 Exerts Protective Effect in Oxidative Stress and Liver Dysfunctions Resulting from Experimental Sepsis.

Background: Sepsis is a severe global health problem, with high morbidity and mortality. In sepsis, one of the main affected organs is the liver. Hepatic alterations characterize a negative prognostic. Omega-3 fatty acids (ω3), eicosapentaenoic acid, and docosahexaenoic acid, are part of the main families of polyunsaturated fatty acids. ω3 has been used in studies as sepsis treatment and as a treatment for non-alcoholic liver disease. Aim: We aimed to evaluate the effects of treatment with fish oil (FO) rich in ω3 on liver changes and damage resulting from experimental sepsis. Methodology: A model of severe sepsis in Wistar rats was used. Oxidative stress in the liver tissue was evaluated by means of tests of thiobarbituric acid reactive substances, 2,7-dihydrodichlorofluorescein diacetate , catalase, and glutathione peroxidase, in the serum TBARS, DCF, thiols and, to assess liver dysfunction, alanine aminotransferase and aspartate aminotransferase. Hepatic tissue damage was evaluated using H&E histology. Results: In assessments of oxidative stress in liver tissue, a protective effect was observed in the tests of TBARS, DCF, CAT, and GPx, when compared the sepsis versus sepsis+ω3 groups. Regarding the oxidative stress in serum, a protective effect of treatment with ω3 was observed in the TBARS, DCF, and thiols assays, in the comparison between the sepsis and sepsis+ω3 groups. ω3 had also a beneficial effect on biochemical parameters in serum in the analysis of ALT, creatinine, urea, and lactate, observed in the comparison between the sepsis and sepsis+ω3 groups. Conclusion: The results suggest ω3 as a liver protector during sepsis with an antioxidant effect, alleviating injuries and dysfunctions.

Neuroinflammatory responses following zinc or branched-chain amino acids supplementation in obese rats.

The excessive production of pro-inflammatory mediators, characteristic of obesity, leads to neuroinflammation. Zinc (Zn) and the branched-chain amino acids (BCAA) are supplements known for their immunomodulatory properties. Our goal was to evaluate if Zn or BCAA supplementation can affect long-term recognition memory and neuroinflammatory parameters of obese rats after a high-fat diet (HFD). Three-month-old Wistar rats were divided into six groups: Standard diet (SD) + vehicle; SD + Zn; SD + BCAA; High-fat diet (HFD) + vehicle; HFD + Zn; and HFD + BCAA. Diets were administrated for 19 weeks, Zn (1,2 mg/kg/day) or BCAA (750 mg/kg/day) supplementation was conducted in the last 4 weeks. Long-term recognition memory was evaluated by the novel object recognition test. IL-1ß immunoreactivity in the cortex and hippocampus, and IL-6 levels in the cortex tissue were assessed. Astrogliosis were evaluated through GFAP + cell count and morphological analysis (Sholl Method). Zn supplementation improved object recognition memory in HFD-fed rats, which was not observed following BCAA supplementation. The levels of IL-6 in the cerebral cortex were higher after HFD, which was not diminished after neither supplementation. Obesity also led to increased IL-1ß immunoreactivity in the cerebral cortex and hippocampus, which was reduced by Zn. BCAA supplementation also diminished IL-1ß immunoreactivity, but only in the hippocampus. We also showed that astrocyte reactivity caused by HFD is area-dependent, being the cerebral cortex more susceptible to the diet. Even though BCAA and Zn can affect IL-1ß immunoreactivity and astrocyte morphology, only Zn improved memory. Future studies are needed to clarify the pathways by which Zn improves cognition in obesity.

DHA/EPA supplementation decreases anxiety-like behaviour, but it does not ameliorate metabolic profile in obese male rats.

Obesity is a major public health problem that predisposes to several diseases and higher mortality in patients with COVID-19. Obesity also generates neuroinflammation, which predisposes to the development of neuropsychiatric diseases. Since there is a lack of effective treatments for obesity, the search for new strategies to reverse its consequences is urgent. In this perspective, the anti-inflammatory properties of omega-3 polyunsaturated fatty acids such as DHA/EPA might reduce the harmful effects of obesity. Here, we used the cafeteria diet (CAF) model to induce obesity in Wistar rats. Animals received ultra-processed food for 20 weeks, and DHA/EPA supplementation (500 mg/kg per d) was performed between the 16th and the 20th week. At the end of the experiment, it was evaluated: body weight, visceral fat deposition, plasma glucose, insulin and triglycerides, and it was also measured the levels of inflammatory cytokines TNF-α and IL-6 in plasma and liver, and TNF-α in the prefrontal cortex. The elevated plus maze test was performed to analyse anxiety-like behaviour. Our results demonstrated that DHA/EPA could not reverse weight and fat gain and did not modify plasma dosages. However, there was a decrease in IL-6 in the liver (DHA/EPA effect: P = 0.023) and TNF-α in the brain (CAF compared with CAF + DHA/EPA, P < 0.05). Also, there was a decrease in the anxiety index in CAF + DHA/EPA compared with the CAF group (P < 0.01). Thus, DHA/EPA supplementation is helpful to reverse the consequences of obesity in the brain.

Zinc Supplementation Decreases Obesity-Related Neuroinflammation and Improves Metabolic Function and Memory in Rats.

OBJECTIVE: The purpose of this study was to evaluate the effects of zinc (Zn) supplementation on metabolic and neuroinflammatory parameters in cafeteria diet (CAF)-induced obesity in Wistar rats. METHODS: Animals were divided into four groups: control diet (CT); CT+Zn; CAF; CAF+Zn. The diet was administered for 20 weeks; Zn treatment (10 mg/kg/d) started at week 16 and it was conducted until the end of the diet protocol. Weight gain, visceral fat, and plasma levels of glucose, triglycerides, insulin, TNF-α, and IL-6, as well as homeostatic model assessment of insulin resistance, were assessed. Glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor molecule 1 (Iba-1) expression in the cerebral cortex and toll-like receptor 4 (TLR-4) in the cerebral cortex and hippocampus were evaluated. Memory was assessed by the novel object recognition test. RESULTS: CAF diet increased weight gain, visceral fat, and plasma glucose, triglyceride, and TNF-α levels. Zn reversed the hyperglycemia caused by CAF diet and reduced IL-6 levels. In the cerebral cortex, GFAP was similar between groups; Iba-1 was increased by CAF diet but reduced in the CAF+Zn group. Zn reduced CAF-dependent TLR-4 increase in the hippocampus but not in the cerebral cortex. CAF-fed animals showed impaired recognition memory, whereas Zn reversed it. CONCLUSIONS: These findings demonstrate that Zn partially reverted obesity-related metabolic dysfunction and reduced neuroinflammation and memory deficit caused by CAF diet.

Altered expression of COX-2 and TNF-α in patients with hepatocellular carcinoma.

BACKGROUND AND AIM: hepatocellular carcinoma is a type of cancer related with inflammation, as 90% of cases develop in a chronic inflammation condition. Excess inflammation can affect tissue homeostasis. Cytokines and inflammatory mediators are immunological components that can influence the functioning of cells and tissues. In addition, the estrogen receptor appears to play an important role in hepatocarcinogenesis. The aim of the study was to evaluate the expression of inflammatory markers and ER in patients with hepatocellular carcinoma. METHODS: data from 143 patients of ISCMPA were analyzed. Immunohistochemistry was performed of cyclooxygenase-2 enzyme (COX-2), nuclear factor kappa B (NF-κB), tumor necrosis factor alpha (TNF-α) and ER in paraffin-embedded hepatic tissue. The percentage of the stained area, intensity of staining and of the number of ER positive nuclei were evaluated using the ImageJ 1.50 software. RESULTS AND CONCLUSION: there was a significant difference between the groups in terms of the percentage of marked area (p = 0.040) for COX-2 and the intensity of staining of TNF-α (p = 0.030). No significant differences were observed in any of other parameters evaluated. In conclusion, COX-2 and TNF-α are possible markers that should be further studied to determine their immunohistochemical profile and role in HCC development.

Maternal feeding associated to post-weaning diet affects metabolic and behavioral parameters in female offspring.

Genetic and environmental factors related to maternal diet may predispose offspring to serious diseases. However, consequences of a maternal diet intervention during gestation and lactation, and its association with caloric restriction after weaning on the progeny are not completely known. In this context, the goal of the present study was to investigate how different maternal diets, control (CONT), hypercaloric (HD) or restrictive (RD) diets during gestation and lactation, may affect the metabolism and behavior of the offspring that was also submitted to RD. Experimental groups were abbreviated accordingly maternal/offspring diets: CONT/CONT, CONT/RD, RD/CONT, RD/RD, HD/CONT, HD/RD. Our results showed that glucose serum concentration is increased in mice from dams fed a HD. However, offspring from RD-fed dams showed lower insulin and leptin levels than the other groups, indicating a maternal diet effect. Moreover, animals from RD/CONT group showed a higher adipocyte area in comparison to both HD/CONT and CON/CONT. Offspring from RD-fed dams exhibited a decrease in lateral area locomotion in the open field test. Evaluation of anxiety-like behavior and recognition memory showed no significant difference among groups. Thus, maternal RD provides a beneficial response in metabolic parameters, but its effects on behavior is not completely clarified.

Omega-3 fatty acids revert high-fat diet-induced neuroinflammation but not recognition memory impairment in rats.

Neuroinflammation is a consequence of overeating and may predispose to the development of cognitive decline and neurological disorders. This study aimed to evaluate the impact of omega-3 supplementation on memory and neuroinflammatory markers in rats fed a high-fat diet. Male Wistar rats were divided into four groups: standard diet (SD); standard diet + omega-3 (SD + O); high fat diet (HFD); and high fat diet + omega-3 (HFD + O). Diet administration was performed for 20 weeks and omega-3 supplementation started at the 16th week. HFD significantly increased body weight, while omega-3 supplementation did not modify the total weight gain. However, animals from the HFD + O group showed a lower level of visceral fat along with an improvement in insulin sensitivity following HFD. Thus, our results demonstrate a beneficial metabolic role of omega-3 following HFD. On the other hand, HFD animals presented an impairment in object recognition memory, which was not recovered by omega-3. In addition, there was an increase in GFAP-positive cells in the cerebral cortex of the HFD group, showing that omega-3 supplementation can be effective to decrease astrogliosis. However, no differences in GFAP number of cells were found in the hippocampus. We also demonstrated a significant increase in gene expression of pro-inflammatory cytokines IL-6 and TNF-α in cerebral cortex of the HFD group, reinforcing the anti-inflammatory role of this family of fatty acids. In summary, omega-3 supplementation was not sufficient to reverse the memory deficit caused by HFD, although it played an important role in reducing the neuroinflammatory profile. Therefore, omega-3 fatty acids may play an important role in the central nervous system, preventing the progression of neuroinflammation in obesity.

Cirrhosis inducss apoptosis in renal tissue through intracellular oxidative stress / Cirrose induz apoptose em tecido renal através de estresse oxidativo intracelular

Background Renal failure is a frequent and serious complication in patients with decompensated cirrhosis. Objectives We aimed to evaluate the renal oxidative stress, cell damage and impaired cell function in animal model of cirrhosis. Methods Secondary biliary cirrhosis was induced in rats by ligation of the common bile duct. We measured TBARS, ROS and mitochondrial membrane potential in kidney as markers of oxidative stress, and activities of the antioxidant enzymes. Relative cell viability was determined by trypan blue dye-exclusion assay. Annexin V-PE was used with a vital dye, 7-AAD, to distinguish apoptotic from necrotic cells and comet assay was used for determined DNA integrity in single cells. Results In bile duct ligation animals there was significant increase in the kidney lipoperoxidation and an increase of the level of intracellular ROS. There was too an increase in the activity of all antioxidant enzymes evaluated in the kidney. The percentage viability was above 90% in the control group and in bile duct ligation was 64.66% and the dominant cell death type was apoptosis. DNA damage was observed in the bile duct ligation. There was a decreased in the mitochondrial membrane potential from 71.40% ± 6.35% to 34.48% ± 11.40% in bile duct ligation. Conclusions These results indicate that intracellular increase of ROS cause damage in the DNA and apoptosis getting worse the renal function in cirrhosis. .

Contexto A falência renal é uma complicação grave e frequente em pacientes com cirrose descompensada. Objetivo Avaliar o estresse oxidativo, o dano ao DNA e alterações na função celular no rim em um modelo animal de cirrose. Métodos A cirrose biliar secundária foi induzida em ratos através da ligadura do duto biliar comum. Foi medido no rim o TBARS (substâncias que reagem ao ácido tiobarbitúrico), ERO (espécies reativas de oxigênio), o potencial de membrana mitocondrial e a atividade das enzimas antioxidantes. A viabilidade celular foi determinada utilizando o ensaio de exclusão do trypan-blue. Para distinguir células em apoptose ou necrose foram usados os marcadores: Anexina V-PE e 7-AAD e o ensaio cometa foi utilizado para determinar dano ao DNA. Resultados Em animais cirróticos houve um aumento significativo da lipoperoxidação no rim e na quantidade de ERO intracelular. Foi observado um aumento na atividade de todas as enzimas antioxidantes. A porcentagem de viabilidade celular foi superior a 90% no grupo controle e de 64,66% no grupo da ligadura do duto biliar. O padrão de morte celular predominante foi apoptose e houve dano ao DNA no grupo da ligadura do duto biliar. Observou-se uma redução no potencial de membrana mitocondrial no grupo da ligadura do duto biliar (34,48% ± 11,40%) em comparação aos controles (71,40% ± 6,35%). Conclusão Esses resultados parecem indicar que nos animais cirróticos ocorre um aumento no dano oxidativo e ao DNA levando as células renais à apoptose, o que contribui para a falência renal na cirrose. .

The effect of celecoxib on the development of diethylnitrosamine-induced liver tumors in rats.

BACKGROUND/AIMS: Hepatocellular carcinoma is one of the most commonly diagnosed malignant tumors in the world, and it typically has a poor prognosis. Extensive studies have examined the effects of non-steroidal anti-inflammatory drugs selective to COX-2 on the chemoprevention of various tumors. The objective of this study is to observe the effect of celecoxib on the development of liver tumors in rats. MATERIAL AND METHODS: Hepatocellular carcinoma was induced in a group of 75 rats with the carcinogen diethylnitrosamine. The animals were divided into 5 groups. Three groups received various doses of celecoxib, one group received indomethacin, and a control group received no non-steroidal selective anti inflammatory drugs. RESULTS: The experimental model was considered to be successful because 78% of the rats in the control group developed liver tumors. The number of neoplastic lesions was similar among the celecoxib, indomethacin and control groups, although the nodule diameter of the lesions was smaller in the celecoxib group. Better results were observed in animals that received celecoxib at doses of 6 and 9 mg/kg/ day; 4 rats in these groups did not show any neoplastic histological lesions, and a greater proportion of the nodules in the other animals in these groups were benign than in the groups that did not use celecoxib. CONCLUSIONS: These results suggest that celecoxib may play a role in modifying the natural history of hepatocellular carcinoma development.

Treatment with aqueous extract from Croton cajucara Benth reduces hepatic oxidative stress in streptozotocin-diabetic rats.

Croton cajucara Benth is a plant found in Amazonia, Brazil and the bark and leaf infusion of this plant have been popularly used to treat diabetes and hepatic disorders. The present study was designed to evaluate the oxidative stress as well as the therapeutic effect of Croton cajucara Benth (1.5 mL of the C. cajucara extract i.g.) in rats with streptozotocin-induced diabetes. Croton cajucara Benth was tested as an aqueous extract for its phytochemical composition, and its antioxidant activity in vitro was also evaluated. Lipid peroxidation and superoxide dismutase, catalase, and glutathione reductase activities were measured in the hepatic tissue, as well as the presence activation of p65 (NF-κB), through western blot. Phytochemical screening of Croton cajucara Benth detected the presence of flavonoids, coumarins and alkaloids. The extract exhibited a significant antioxidant activity in the DPPH-scavenging and the hypoxanthine/xanthine oxidase assays. Liver lipid peroxidation increased in diabetic animals followed by a reduction in the Croton-cajucara-Benth-treated group. There was activation of p65 nuclear expression in the diabetic animals, which was attenuated in the animals receiving the Croton cajucara Benth aqueous extract. The liver tissue in diabetic rats showed oxidative alterations related to the streptozotocin treatment. In conclusion the Croton cajucara Benth aqueus extract treatment effectively reduced the oxidative stress and contributed to tissue recovery.

Hepatic nitrosative stress in experimental diabetes.

AIM: The effects of the inhibition of nitrosative stress by aminoguanidine in an experimental model of diabetes mellitus (DM) were investigated. METHODS: Twenty-one male Wistar rats were divided into three groups: control (CO), diabetic (DM), and diabetic treated with aminoguanidine (DM+AG). Aminoguanidine (aminoguanidine hemisulfate salt, Sigma Chemical Co., St. Louis, MO, USA) was used at a dose of 50 mg/kg (i.p.) during the last 30 days of the experiment. The expression levels of liver lipoperoxidation (TBARS - nmol/mg protein), inducible oxide nitric synthase (iNOS), nitrotyrosine and the NFκB nuclear transcription factor p65 were examined using western blot analysis. RESULTS: The DM group demonstrated an increase in lipoperoxidation and in the expression of iNOS, nitrotyrosine and p65. Aminoguanidine reduced hepatic lipid peroxidation and protein expression levels of iNOS, nitrotyrosine and p65. CONCLUSION: Aminoguanidine treatment reduces liver oxidative and nitrosative stress in diabetic animals. In addition, aminoguanidine reduced the expression of p65 in the liver.

The effect of taurine on hepatic steatosis induced by thioacetamide in zebrafish (Danio rerio).

BACKGROUND: Nonalcoholic fatty liver disease is one of the most prevalent forms of chronic liver disease in the Western world. Taurine is a conditionally essential amino acid in humans that may be a promising therapy for treating this disease. AIM: To evaluate the effect of taurine on hepatic steatosis induced by thioacetamide in Danio rerio. METHODS: Animals were divided into four groups: control (20 µl of saline solution), taurine (1,000 mg/kg), thioacetamide (300 mg/kg), and the taurine-thioacetamide group (1,000 + 300 mg/kg). Thioacetamide was injected intraperitoneally three times a week for 2 weeks. The mRNA expression, lipoperoxidation, antioxidant enzymatic activity, and histological analyses were evaluated in the liver and the triglyceride content was assessed in the serum. RESULTS: Thioacetamide injection induced steatosis, as indicated by histological analyses. The lipoperoxidation showed significant lipid damage in the thioacetamide group compared to the taurine-thioacetamide group (p < 0.001). Superoxide dismutase (SOD) activity in the taurine-thioacetamide group (5.95 ± 0.40) was significantly increased compared to the thioacetamide group (4.14 ± 0.18 U SOD/mg of protein) (p < 0.001). The mRNA expression of SIRT1 (0.5-fold) and Adiponectin receptor 2 (0.39-fold) were lower in the thioacetamide group than the control (p < 0.05). TNF-α mRNA expression was 6.4-fold higher in the thioacetamide group than the control (p < 0.05). SIRT1 mRNA expression was 2.6-fold higher in the taurine-thioacetamide group than in the thioacetamide group. CONCLUSIONS: Taurine seems to improve hepatic steatosis by reducing oxidative stress and increasing SIRT1 expression.

Hepatics alterations and genotoxic effects of Croton cajucara Benth (SACACA) in diabetic rats / Alterações hepáticas e efeitos genotóxicos do Croton cajucara Benth (SACACA) em ratos diabéticos

CONTEXT: Croton cajucara Benth is a plant found in Amazonia, Brazil and the bark and leaf infusions of this plant have been popularly used to treat diabetes and hepatic disorders. OBJECTIVES: This study investigated effects hepatics alterations and genotoxic and antidiabetic effect of Croton cajucara Benth bark extracts treatment in streptozotocin-induced diabetic rats. METHODS: Male Wistar rats were divided into six groups: control rats; control rats treated with Croton cajucara Benth extract during 5 and 20 days; diabetic rats, and diabetic rats treated with Croton cajucara Benth during 5 and 20 days. Diabetes was induced by a single intraperitoneal injection of streptozotocin (70 mg/kg). Eight weeks later we measured glucose, triglyceride, cholesterol and hepatic transaminases on blood. The bone marrow micronucleus assay was used to assess the genotoxic activity of Croton cajucara Benth. RESULTS: Treatment with aqueous extrat of Croton cajucara was able to significantly reduce levels of triglycerides in diabetic animals, however, did not modify significantly the levels of glucose and cholesterol in these animals. There was no significant elevation in liver transaminases in the control group treated with Croton cajucara Benth, as there was no genotoxic effect of treatment in this model. Our results did not show a significant effect on glucose and cholesterol reduction, the treatment was able to significantly reduce triclycerides plasmatic level. There was no significant alterations on hepatic transferase in the animals from the control group treated with Croton cajucara Benth. It was observed no genotoxic effect of the treatment in the model studied. CONCLUSION: In this study Croton cajucara bark extract showed absence of hepatotoxicity in this animal model and presented a hypolipidemic activity, and could be used to reverse dyslipidemia associated with diabetes and to prevent the cardiovascular complications that are very prevalent in diabetic patients.

CONTEXTO: Croton cajucara Benth é uma planta encontrada na Amazônia, Brasil. Infusões da casca e folhas desta planta são utilizadas popularmente no tratamento de diabetes e doenças hepáticas. OBJETIVOS: Este estudo investigou as alterações hepáticas e os efeitos genotóxicos da casca do extrato do Croton cajucara Benth em animais diabéticos induzidos por estreptozotocina. MÉTODOS: Ratos Wistar machos foram divididos em seis grupos: ratos controle, ratos controle tratados com extrato de Croton cajucara Benth durante 5 e 20 dias, ratos diabéticos e diabéticos tratados com Croton cajucara Benth durante 5 e 20 dias. O diabetes foi induzido por uma única injeção intraperitonial de estreptozotocina (70 mg/kg). Oito semanas mais tarde foram medidos os níveis de glicose, triglicerídios, colesterol e transaminases hepáticas no sangue. O teste do micronúcleo da medula óssea foi utilizado para avaliar a atividade genotóxica do Croton cajucara Benth. RESULTADOS: O tratamento com o extrato aquoso do Croton cajucara foi capaz de reduzir significativamente os níveis plasmásticos dos triglicerídios nos animais diabéticos, porém, não modificaram significativamente os níveis de glicose e colesterol nesses animais. Não houve elevação significativa nas transaminases hepáticas nos animais do grupo controle tratadas com Croton cajucara Benth, assim como também não houve efeito genotóxico do tratamento, no modelo estudado. CONCLUSÃO: O extrato aquoso da casca do Croton cajucara Benth foi hipolipemiante, sugerindo seu uso para prevenir as dislipidemias encontradas em pacientes diabéticos.

Effects of dermal exposure to Nicotiana tabacum (Jean Nicot, 1560) leaves in mouse evaluated by multiple methods and tissues.

Tobacco farmers are routinely exposed to complex mixtures of the compounds present in tobacco leaves, including organic and inorganic pesticides. Penetration through skin is the most significant route of uptake in occupational exposure to chemicals, including dust and liquids containing toxic and carcinogenic substances. This study evaluates the genotoxic effect of tobacco leaves with and without dermal exposure to flumetralin in Mus musculus, determining cell damage by the micronucleus test and the Comet assay as well as antioxidant enzyme activities and hematologic parameters. Nicotine was used as positive control. Blood samples were collected for 0, 3, 24 and 48 h exposure periods, and DNA damage by Comet assay and micronucleus test was evaluated for all these periods. Bone marrow and liver cells were also evaluated for the 48 h exposure period. Significant differences between Comet assay results in blood cells from animals exposed to tobacco leaves with and without pesticide were found in 24 and 48 h exposure periods in relation to negative control. Bone marrow cells from the group exposed to leaves with pesticide (48 h) also demonstrated significant increase in DNA damage. Concerning the micronucleus test, only animals exposed to tobacco leaves without pesticide (24 h) showed increase in frequency of micronuclei when compared to the negative control. Oxidative stress activities also were demonstrated for different groups. The results demonstrate the injury effect caused by tobacco leaves in different Mus musculus tissues, suggesting that the effects of dermal exposure to tobacco leaves are caused by complex mixtures present in the plant, but mainly by nicotine.

Aminoguanidina reduz o estresse oxidativo e as alterações estruturais pulmonares em diabetes mellitus experimental / Aminoguanidine reduces oxidative stress and structural lung changes in experimental diabetes mellitus

Avaliamos o efeito da aminoguanidina sobre o estresse oxidativo pulmonar e a estrutura pulmonar em um modelo experimental de diabetes mellitus. Foram determinados thiobarbituric acid reactive substances (TBARS, substâncias reativas ao ácido tiobarbitúrico), histologia e gasometria arterial em animais com diabetes mellitus (DM), animais com diabetes mellitus tratados com aminoguanidina (DM+AG) e controles. O nível de TBARS foi significativamente maior no grupo DM que nos grupos controle e DM+AG (2,90 ± 1,12 vs. 1,62 ± 0,28 e 1,68 ± 0,04 nmol/mg proteína, respectivamente), o mesmo ocorrendo com PaCO2 em relação ao grupo controle (49,2 ± 1,65 vs. 38,12 ± 4,85 mmHg), e PaO2 foi significativamente maior no grupo controle (104,5 ± 6,3 vs. 69,48 ±16,30 e 97,05 ± 14,02 mmHg, respectivamente). Neste modelo experimental de diabetes mellitus, a aminoguanidina reduziu o estresse oxidativo, alterações estruturais teciduais pulmonares e a troca gasosa no modelo experimental.

We evaluated the effect of aminoguanidine on pulmonary oxidative stress and lung structure in an experimental model of diabetes mellitus. Thiobarbituric acid reactive substances (TBARS), histology and arterial blood gases were evaluated in animals with diabetes mellitus (DM group), animals with diabetes mellitus treated with aminoguanidine (DM+AG group), and controls. The TBARS levels were significantly higher in the DM group than in the control and DM+AG groups (2.90 ± 1.12 vs. 1.62 ± 0.28 and 1.68 ± 0.04 nmol/mg protein, respectively), as was PaCO2 when compared with that of the control group (49.2 ± 1.65 vs. 38.12 ± 4.85 mmHg), and PaO2 was significantly higher in the control group (104.5 ± 6.3 vs. 16.30 ± 69.48 and 97.05±14.02 mmHg, respectively). In this experimental model of diabetes mellitus, aminoguanidine reduced oxidative stress, structural tissue alterations, and gas exchange.

Estresse oxidativo e alterações estruturais pulmonares no diabetes mellitus experimental / Experimental diabetes mellitus: oxidative stress and changes in lung structure

O diabetes mellitus é uma desordem endócrino-metabólica caracterizada pela hiperglicemia. O seu impacto no sistema respiratório é caracterizado por alterações funcionais e na troca gasosa. O objetivo deste estudo foi avaliar o aumento do estresse oxidativo e os possíveis danos na estrutura pulmonar no modelo de diabetes experimental induzido por estreptozotocina. Foram realizadas análises histológicas, bioquímicas e gasométricas no pulmão de ratos diabéticos. Concluiu-se que o estresse oxidativo está presente no diabetes mellitus experimental e que ocorrem alterações estruturais no tecido pulmonar, bem como alterações na troca gasosa.

Diabetes mellitus is an endocrine/metabolic disorder characterized by hyperglycemia. Its impact on the respiratory system is characterized by functional changes and alterations in gas exchange. The objective of this study was to evaluate the increase in oxidative stress and the potential damages to the lung structure in an experimental model of streptozotocin-induced diabetes. We conducted histological, biochemical and blood gas analyses in the lungs of diabetic rats. We concluded that the effects of experimental diabetes mellitus include oxidative stress, structural changes in the lung tissue and altered gas exchange.

Implementação de um novo modelo de experimentação animal: Zebrafish / Implementation of a new experimental animal model: Zebrafish

O Danio rerio (zebrafish, paulistinha) é um pequeno peixe de água-doce, que vem sendo utilizado como modelo de animal para o estudo de numerosas doenças humanas. A sua facilidade de manutenção e reprodução e os métodos laboratoriais para sua criação já estão bem estabelecidos. Sua manutenção requer alguns cuidados básicos e a compra de equipamentos específicos, porém estes são de baixo custo. Este peixe é considerado um bom modelo para o estudo de doenças humanas, pode servir como uma relevante plataforma para estudo de eventos moleculares, estratégias terapêuticas e avaliação dos mecanismos fisiológicos de algumas patologias. O Laboratório Experimental de Hepatologia e Gastroenterologia (LEHG), do Centro de Pesquisas do Hospital de Clínicas de Porto Alegre, iniciou em 2008 estudos na área da Hepatologia com o Zebrafish, aqui apresentados.

Danio rerio (zebrafish, paulistinha) is a freshwater small fish that has been used as an animal model for studies of several human diseases. Its characteristics of being easily bred and reproduced and its laboratory housing methods are well established. It requires some basic care and the acquisition of specific low-cost equipment. Since this fish has already been considered a good human disease model, it may serve as a powerful preclinical platform for the study of molecular events, therapeutic strategies, and for evaluating the physiological mechanisms of some pathologies. The Laboratory of Experimental Hepatology and Gastroenterology (LEHG) of the Research Center of Hospital de Clínicas de Porto Alegre initiated studies with the zebrafish in 2008, presented here.