Anti-hyperlipidemic effects of Campomanesia xanthocarpa aqueous extract and its modulation on oxidative stress and genomic instability in Wistar rats.

The use of natural products from herbs may be a therapeutic option in dyslipidemia treatment. Campomanesia xanthocarpa (Mart.) O. Berg (Myrtaceae) leaves have been used to decrease cholesterol levels. However, studies to determine activities of this plant on triglycerides metabolism have received little attention. The aim of this study was to examine anti-hyperlipidemic effects of a C. xanthocarpa aqueous leaf extract (CxAE) and assess protective actions against oxidative stress and DNA damage. The tyloxapol-induced hyperlipidemia model was used in Wistar rats. Rats were treated orally with CxAE either 250 or 500 mg/kg/day for 7 days prior to tyloxapol administration. Biochemical parameters, oxidative stress levels, and genomic instability were assessed in several tissues. CxAE decreased cholesterol and triglyceride levels in serum and hepatic and renal DNA damage in tyloxapol-treated rats. There was no marked effect on the micronucleus frequency in bone marrow. The extract increased catalase activity and decreased glutathione S-transferase activity in kidney tissue. CxAE showed anti-hyperlipidemic effects, improved oxidative parameters, and protected DNA against damage induced by tyloxapol-induced hyperlipidemia, suggesting C. xanthocarpa leaves may be useful in preventing dyslipidemias.Abbreviations: ALP: Alkaline phosphatase; ALT: Aspartate aminotransferase; ANOVA: Analysis of variance; AST: Aspartate aminotransferase; Ator: Atorvastatin; CAT: Catalase; Chol: Cholesterol; CxAE: Campomanesia xanthocarpa aqueous extract; GST: Glutathione S-transferase; HDL: High density cholesterol; i.p.: Intraperitoneal; NCE: Normochromatic erythrocyte; PBS: Phosphate buffer solution; PCE: Polychromatic erythrocyte; ROS: Reactive oxygen species; SD: Standard deviation; SOD: Superoxide dismutase; T: Tyloxapol; TBARS: Thiobarbituric acid reacting substances; TG: Triglyceride.

Toxicological aspects of Campomanesia xanthocarpa Berg. associated with its phytochemical profile.

Campomanesia xanthocarpa leaves are used as tea to treat diarrhea, inflammation, and hypercholesterolemia. Some pharmacological studies noted its beneficial uses of C. xanthocarpa; however, few investigations examined the toxicological profile of this plant. The aim of this study was to determine the chemical composition, genotoxic, and mutagenic potential of an aqueous extract of C. xanthocarpa leaves (CxAE), and potential protective effects against oxidative damage. Phytochemical constituents were determined using HPLC, and antioxidant effect in vitro was measured using 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radical assay. Genotoxic effects and chromosomic mutations were assessed using comet assay and micronucleus (MN) test in Wistar rats treated with CxAE at 250, 500 or 1000 mg/kg for 7 consecutive days. Lipid peroxidation and antioxidant enzyme activities were measured in several tissues. CxAE induced mutations in TA98, TA97a, and TA102 strains. However, in the presence of metabolic activation, data were negative for all strains tested. Lack of mutagenicity was also observed in the MN test. This extract did not induce DNA damage, except when the highest concentration was used. DNA oxidative damage induced by hydrogen peroxide (H2O2) decreased in blood after treatment with CxAE. Lipid peroxidation levels were reduced while superoxide dismutase (SOD) activity increased in kidneys. The inhibitory concentration of CxAE required to lower DPPH levels to 50% was 38.47 ± 2.06 µg/ml. In conclusion, frameshift and oxidative mutations were observed only in the absence of metabolic activation which may be attributed to the presence of flavonoids such as quercetin. It is of interest that CxAE also showed protective effects against DNA oxidative damage associated with presence of ellagic acid, a phenolic acid with antioxidant activities. CxAE did not induce in vivo mutagenicity, suggesting that this extract poses a low toxic hazard over the short term.

Anti-inflammatory and antioxidant effect of melatonin on recovery from muscular trauma induced in rats.

In recent decades, the number of people who practice sports has grown exponentially, increasing the number of muscular injuries. Trauma injury occurs when the muscle is exposed to a sudden compression force. Melatonin (MLT) has often been cited in the literature as a potent antioxidant and anti-inflammatory agent. This study was designed to evaluate MLT action on muscle tissue in Wistar rats in an experimental model of muscle trauma. Twenty-eight Wistar rats were used, divided into four groups: CO (Control), CO + MLT (Control + Melatonin), T (Trauma) and T + MLT (Trauma + Melatonin). MLT (20 mg/kg) was administered (ip) daily at dusk until day 7. The trauma occurred on day 1, 2 h before the first MLT application. On day 8, muscle tissue was collected for histological analysis (HE), immunohistochemistry (TNF-α and NFκB), evaluation of oxidative stress through analysis of lipoperoxidation by TBARS and activity of SOD and GPx enzymes, and analysis of nitrites and nitrates. In the evaluation of TBARS and SOD, we observed a significant increase in the T group and a significant decrease in the T + MLT group. In the evaluation of GPx, there was a significant increase in the T group and a significant decrease in the T + MLT group. The histological analysis of muscle tissue revealed structural changes of muscle fibers and inflammatory infiltrate in the T group but a decrease in this damage in the T + MLT group. In the immunohistochemical evaluation, increased expression of TNFα and NFκB proteins in the T group was observed and a significant decrease of this expression in the T + MLT group. MLT was shown to attenuate oxidative damage and to diminish the expression of inflammatory proteins and tissue damage in this experimental model.

Zinc supplementation reduces diet-induced obesity and improves insulin sensitivity in rats.

Rates of obesity have been growing at alarming rates, compromising the health of the world population. Thus, the search for interventions that address the metabolic repercussions of obesity are necessary. Here we evaluated the metabolic and antioxidant effects of zinc and branched-chain amino acids (BCAA) supplementation on obese rats. Male Wistar rats were fed either a high-fat/high-fructose diet (HFD) or a standard diet (SD) for 19 weeks. From the fifteenth week until the end of the experiment, HFD- and SD-fed rats received zinc (6 mg/kg) or BCAA (750 mg/kg) supplementation. Body weight, abdominal fat, lipid profile, blood glucose, insulin, leptin, and hepatic transaminases were evaluated. In the liver, superoxide dismutase and catalase activities and lipid peroxidation were also analyzed. HFD-fed animals showed increased weight gain, abdominal fat pad, plasma insulin, leptin, and triglycerides levels in comparison with SD-fed rats. Zinc supplementation reduced all these parameters, suggesting a beneficial role for the treatment of obesity. BCAA, on the other hand, did not show any beneficial effect. Liver antioxidant enzymes and hepatic transaminases plasma levels did not change among groups. Lipid peroxidation was higher in HFD-fed rats and was not reverted by zinc or BCAA supplementation. In conclusion, zinc supplementation may be a useful strategy for the treatment of the metabolic dysfunction associated with obesity.

Protective effects of quercetin treatment in a pristane-induced mouse model of lupus nephritis.

INTRODUCTION: Lupus nephritis (LN) is one of the most severe complications of systemic lupus erythematosus. As murine models of LN are valuable tools to better understand its pathophysiology and to search for new effective treatments, we investigated the effects of the bioflavonoid quercetin on pristane-induced LN mice through histomorphological analyses. METHODS: Immunofluorescence and biochemical assays were used to evaluate the expression of markers of inflammation (interleukin-6, IL-6; tumour necrosis factor-α, TNF-α), oxidative stress (catalase, CAT; superoxide dismutase 1, SOD1; thiobarbituric acid reactive substances, TBARS), apoptosis (Bax), and fibrosis (transforming growth factor-ß1, TGF-ß1). Glomerular and tubular ultrastructure was analysed, and tissue messenger RNA of podocin, podoplanin and α3ß1-integrin were quantified using the real-time polymerase chain reaction. RESULTS: Pristane-induced LN mice showed severe kidney injury, characterized by increased proteinuria, glomerular mesangial expansion and inflammation, high expression of the pro-fibrotic, apoptotic and prooxidant markers and reduction of antioxidants. In the kidney ultrastructure, foot process (FP) effacement, apoptotic mesangial cells and abnormal mitochondria with disrupted cristae were observed, along with suppressed tissue mRNA of podocin, podoplanin and α3ß1-integrin. Treatment with quercetin in the pristane-induced LN mice model was nephroprotective, decreasing proteinuria levels and significantly lowering tissue expression of IL-6, TNF-α, TGF-ß1, Bax and TBARS. Simultaneously, quercetin significantly increased CAT and SOD1 expressions in these mice. In addition, it was observed improvement of the kidney ultrastructure, and tissue mRNA of podocin, but not podoplanin and α3ß1-integrin, was restored to the levels found in the control mice. CONCLUSION: In conclusion, these findings provide experimental evidence of the renoprotective effects of quercetin in the pristane-induced LN mice model. We suggest that quercetin effectively ameliorates the kidney damage caused by pristane, a bioflavonoid to be further evaluated as a new therapeutic strategy in this disease.

Protective effect of glutamine on the main and adjacent organs damaged by ischemia-reperfusion in rats.

Intestinal ischemia and reperfusion (I/R) causes cellular and tissue damage to the intestine and remote organs such as the liver. Increased production of ROS and nitric oxide and dysregulation of cytoprotective enzymes may be involved in intestinal I/R. The aim was to evaluate the protective effects of glutamine on the intestine and liver of rats with intestinal I/R injury. Twenty male Wistar rats (300 g) were divided into four groups: sham-operated (SO), glutamine + SO (G + SO), I/R, and glutamine + I/R (G + I/R). Occlusion of the SMA for 30 min was followed by 15-min reperfusion. Glutamine (25 mg/kg/day) was administered once daily 24 and 48 h before I/R induction. Blood and tissue of were collected for aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, histopathological analysis, immunohistochemistry of IL-1ß and TNF-α, thiobarbituric acid reactive substance (TBARS) and nitric oxide, Nrf2/keap1, superoxide dismutase (SOD), NADPH quinone oxidoreductase1 (NQO1), inducible nitric oxide synthase (iNOS), heat shock protein (HSP70), glucose-regulated protein 78 (GRP78), and activating transcription factor 6 (ATF-6) by western blot. Statistic analysis by ANOVA-Student-Newman-Keuls test (mean ± SE) significantly was p < 0.05. Tissue damage, AST, ALT, IL-1ß, TNF-α, TBARS, NO, Keap1, iNOS, GRP78, and ATF-6 expression were significantly lower in the G + I/R group as compared to the I/R group. Expression of Nrf2, SOD, NQO1, and HSP70, was significantly higher in the G + I/R group as compared to I/R group. Pre-treatment with glutamine provided protection against oxidative damage in the intestine and liver in an experimental model of intestinal I/R.

Antioxidant effect of mesalazine in the experimental colitis model induced by acetic acid / Efeito antioxidante da mesalazina no modelo de colite experimental induzida por ácido acético

Abstract Introduction Inflammatory bowel disease (IBD) is characterized by a chronic inflammation of the gastrointestinal tract, without specific cause or pathogen. Objective The effect of mesalazine in a colitis model induced by acetic acid (AA) was evaluated. Methods We used 40 Wistar rats, ±350 g, divided into 4 groups: control (CO); control + mesalazine (CO + M); colitis (CL) and colitis + M (CL + M) at 24 and 48 h of treatment. The animals received the substances by an intracolonic enema of AA 4% and treatment with mesalazine PO 20 mg/kg after colitis induction. Results Mesalazine reduced tissue damage in the gut, normalized sphincter anal pressure levels and decreased lipid peroxidation, metabolites of nitric oxide and iNOS and NF-kB expression in the treated groups in both treatment time points (24 and 48 h), as well as the activity of antioxidant enzymes. Conclusion Mesalazine was effective in reducing tissue damage and oxidative and inflammatory damage, restored antioxidant capacity and increased anal sphincter pressure levels, possibly due to its antioxidant effect.

Resumo Introdução A doença inflamatória intestinal (DII) caracteriza-se por uma inflamação crônica do trato gastrointestinal sem uma causa ou patógeno específico. Objetivo Foi avaliado o efeito da mesalazina no modelo de colite induzida por ácido acético (AA). Material e métodos Foram utilizados 40 ratos wistar, ±350 gramas, divididos em 4 grupos: Controle (CO); Controle + Mesalasina (CO + M); Colite (CL) e Colite + M (CL + M) nos tempos de 24 e 48 horas de tratamento. Os animais foram submetidos à administração intracolônica por enema com solução de AA a 4% e tratamento com mesalazina na dose oral de 20 mg/kg após a indução da colite. Resultados A mesalazina reduziu as lesões teciduais no intestino, normalizou os níveis de pressão anal esfincteriana, reduziu a lipoperoxidação, metabólitos do óxido nítrico e expressão da iNOS e do NF-kB nos grupos tratados em ambos os tempos de tratamento (24 e 48 horas), bem como a atividade das enzimas antioxidantes. Conclusão A mesalazina demonstrou eficácia na redução das lesões teciduais, danos oxidativos e inflamatórios, restabeleceu a capacidade antioxidante e aumentou os níveis de pressão anal esfincteriana, possivelmente pelo seu efeito antioxidante.

Effect of lecithin on oxidative stress in an experimental model of rats colitis induced by acetic acid / Efeito da lecitina sobre o estresse oxidativo no modelo experimental de colite induzida por ácido acético em ratos

Ulcerative colitis (UC) is an inflammatory disease that affects the bowels. Reactive oxygen species (ROS) are involved in the progress of UC. Objective: Evaluate the antioxidant effect of lecithin in an experimental model of acute UC induced by administration of acetic acid (AA) in rats. Methods: Lecithin (0.5 mL/kg/day) administered orally 2 days before and after induction of colitis with 4% AA in a volume of 4 mL. Twenty-five male Wistar rats were divided in 5 groups: control (CO); control + lecithin (CO + LE); colitis (CL); colitis + lecithin (CL + LE); lecithin + colitis (LE + CL). Anal sphincter pressure, LPO (TBARS), and antioxidant activity of enzymes superoxide dismutase (SOD) and catalase (CAT) were measured, and a histological analysis with H&E was performed. Results and discussion: Anal sphincter pressure was significantly smaller in the CO group, lecithin treatment increased it in pre- and post-treated groups. LPO and SOD activity were increased in the CO group and decreased in the lecithin-treated groups. CAT activity was increased in CO group and decreased in lecithin groups. The histological analysis showed damage to the bowels with destruction of crypts, edema, and inflammatory infiltrate. Use of lecithin preserved the crypts and decreased the edema. Conclusion: Ulcerative colitis increased lipid peroxidation, and the use of lecithin was effective reducing damage to the bowels in the model of experimental colitis.

A retocolite ulcerativa (RCUI) é uma doença intestinal inflamatória. Espécies reativas de oxigênio (ERO) estão envolvidas no progresso da RCUI. Objetivo: Avaliar o efeito antioxidante de lecitina em modelo experimental de RCUI induzida pela administração de ácido acético (AA) em ratos. Métodos: A Lecitina (0,5 mL/kg/dia) foi administrada por via oral 2 dias antes e após a indução de colite com AA. Vinte e cinco ratos Wistar machos foram divididos em 5 grupos: controle (CO); controle + lecitina (CO + LE); colite (CL); colite + lecitina (CL + LE); lecitina + colite (LE + CL). Foram avaliadas: pressão do esfíncter anal, lipoperoxidação (LPO), atividade antioxidante das enzimas superóxido dismutase (SOD) e catalase (CAT), e foi realizada uma análise histológica com H&E. Resultados e discussão: A pressão do esfíncter anal foi significativamente menor no grupo CL, o tratamento com lecitina aumentou a pressão nos grupos pré e pós tratados. A LPO e atividade da SOD aumentaram no grupo CL e diminuíram nos grupos tratados com lecitina. A atividade da CAT foi aumentada no grupo CL e diminuiu nos grupos com lecitina. A análise histológica mostrou danos ao intestino com destruição das criptas, edema e infiltrado inflamatório. O uso de lecitina proporcionou uma preservação das criptas e diminuição do edema. Conclusão: A RCUI aumenta a LPO, a utilização de lecitina foi eficaz na redução dos danos ao intestino induzido por AA no modelo de colite experimental.

Boswellia serrata has beneficial anti-inflammatory and antioxidant properties in a model of experimental colitis.

Ulcerative colitis is an inflammatory disease that involves only the colon and rectum, being characterized by leukocyte infiltrate and superficial ulcers in the intestinal mucosa. To evaluate the anti-inflammatory and antioxidant effects of extract from the Boswellia serrata plant in an experimental rat model of acute ulcerative colitis induced by the administration of acetic acid (AA). An extract of B. serrata (34.2 mg/kg/day) was administered by oral gavage for 2 days before and after the induction of colitis with 4 mL of 4% AA. The anal sphincter pressure in the colitis group showed a significant decrease compared to that of the control groups (p < 0.001). The analysis of the values of lipid peroxidation (LPO) obtained by substances that react with thiobarbituric acid (TBARS) showed a significantly increased LPO in the colitis group compared to the control groups (p < 0.001). The nitric oxide levels and the expression of inducible nitric oxide synthase (iNOS) showed a significant increase in the colitis group compared to control groups (p < 0.01). Both pretreatment and treatment with B. serrata exhibited significantly reduced lipid peroxidation, nitric oxide and iNOS and showed improvements in tissue injury and anal sphincter pressure in animals with ulcerative colitis. The B. serrata extract has protective anti-inflammatory and antioxidant effects that inhibit inflammatory mediators in acute experimental colitis.

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.

Effect of Boswellia serrata on antioxidant status in an experimental model of colitis rats induced by acetic acid.

AIM OF THE STUDY: To evaluate the antioxidant effect of an extract of the plant Boswellia serrata in an experimental model of acute ulcerative colitis induced by administration of acetic acid (AA) in rats. MATERIALS AND METHODS: The extract of B. serrata (34.2 mg/kg/day) was administered orally by gavage for 2 days before and after induction of colitis with AA diluted to 4 % and in a volume of 4 ml. RESULTS: The anal sphincter pressure in the groups treated with B. serrata showed a significant increase compared to the colitis group (P < 0.001). Histological analysis of treated animals showed less edema with preservation of mucosal crypts. Lipid peroxidation showed a significant decrease in the treated groups compared to the colitis group (P < 0.001). The superoxide dismutase (SOD) enzyme activity showed a significant reduction in the treated groups compared to the colitis group (P < 0.001), the glutathione peroxidase (GPx) significantly increased in the treated groups compared to colitis group (P < 0.05), and the same was the result for enzyme activity glutathione (GSH; P < 0.05). CONCLUSIONS: The extract of B. serrata has active antioxidant substances that exert protective effects in acute experimental colitis.

Hepatics alterations and genotoxic effects of Croton cajucara Benth (SACACA) in diabetic rats.

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.

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.

O papel do óxido nítrico na pressão anal esfincteriana de ratos submetidos à colite experimental / The role of nitric oxide in sphincteric anal pressure of rats with experimental colitis

O óxido nítrico (NO) é um radical livre sintetizado endogenamente por várias células do nosso organismo. Apresenta um amplo espectro de ações fisiológicas, sendo as mais importantes o seu mecanismo de ação parácrino no relaxamento da musculatura lisa, sua atividade neurotransmissora em vários sistemas e seu envolvimento no processo inflamatório. O NO é sintetizado em diferentes tecidos através da conversão da L-arginina em L-citrulina pela ação da enzima óxido nítrico sintase (NOS). OBJETIVOS: Este estudo tem por objetivo demonstrar o envolvimento do óxido nítrico no processo intestinal inflamatório de ratos Wistar submetidos à colite experimental com ácido acético. MATERIAL E MÉTODOS: Foram utilizados 20 ratos machos Wistar, com peso entre 250 e 350 gramas divididos em dois grupos de 10 animais. Os animais do grupo em estudo foram submetidos à administração intracolônica, por enema, de uma solução de ácido acético diluído a 7 por cento e com volume de 3 ml. O grupo controle recebeu apenas enema de solução salina. Foram avaliados os índices histológicos, a expressão da enzima óxido nítrico sintase (iNOS) e a pressão anal esfincteriana. RESULTADOS: Os índices histológicos apresentaram uma significativa elevação no grupo colite quando comparados ao grupo controle, tanto na avaliação macroscópica quanto na microscópica. A expressão da enzima iNOS também foi significativamente maior no grupo colite quando comparada ao grupo controle. A pressão anal esfincteriana foi significativamente mais baixa no grupo colite na comparação ao grupo controle. CONCLUSÃO: Os animais submetidos à colite experimental apresentam um aumento da expressão da enzima óxido nítrico sintase induzível (i-NOS). Este aumento, associado ao conseqüente aumento do nível de óxido nítrico, ocasiona uma diminuição dos níveis de pressão anal esfincteriana.

The nitric oxide (NO) is a free radical synthesized from some cells of our organism. It presents with an ample specter of physiological actions being the most important its mechanism of action in the relaxation of the smooth musculature, its neurotransmissor activity in some systems and its involvement in the inflammatory process. The NO is synthesized in different tissues by the conversion of the L-arginine in L-citruline with the action of the enzyme nitric oxide sintase(NOS). OBJECTIVES: the aim of this study is to demonstrate the involvement of nitric oxide in the inflammatory intestinal process of Wistar rats submitted to experimental colitis with ascetic acid. MATERIAL AND METHODS: 20 male Wistar rats had been used with weight between 250 and 350 g divided in two groups of 10 animals. The animals of the group in study had been submitted to intracolonic administration, by enema, of a solution with acid ascetic diluted to 7 percent - 3 ml. The control group received only enema with saline solution. The histological scores, the expression of the enzyme nitric oxide sintase (iNOS) and the sphincteric anal pressure had been evaluated. RESULTS: The histological scores had presented a significant rise in the group colitis when compared with the control group in the macroscopic as well as in the microscopical evaluation. The expression of the enzyme iNOS was also significantly higher in the colitis group when compared to the control group. The sphincteric anal pressure was significantly lower in the group colitis when compared to control group. CONCLUSION: The animals submitted to the experimental colitis presented an increase of the iNOS expression. This increase, associated with the consequent increase in nitric oxide level, causes a reduction of the sphincteric anal pressure levels.

Effects of low-level laser therapy (LLLT) on the nuclear factor (NF)-kappaB signaling pathway in traumatized muscle.

BACKGROUND AND OBJECTIVE: To investigate the effects of low-level laser therapy (LLLT) on nuclear factor kappa B (NF-kappaB) activation and inducible nitric oxide synthase (iNOS) expression in an experimental model of muscle trauma. STUDY DESIGN/MATERIALS AND METHODS: Injury to the gastrocnemius muscle in the rat was produced by a single impact blunt trauma. A low-level galium arsenide (Ga-As) laser (904 nm, 45 mW, and 5 J/cm2) was applied for 35 seconds duration, continuously. RESULTS: Histological abnormalities with increase in collagen concentration, and oxidative stress were observed after trauma. This was accompanied by activation of NF-kappaB and upregulation of iNOS expression, whereas protein concentration of I kappa B alpha decreased. These effects were blocked by LLLT. CONCLUSION: LLLT reduced the inflammatory response induced by trauma and was able to block the effects of reactive oxygen species (ROS) release and the activation of NF-kappaB. The associated reduction of iNOS overexpression and collagen production suggest that the NF-kappaB pathway may be a signaling route involved in the pathogenesis of muscle trauma.

Croton cajucara Benth. leaf extract scavenges the stable free radical DPPH and protects against oxidative stress induced by paraquat.

Antioxidant effects of extracts from Croton cajucara BENTH. leaves was investigated in different in vitro and in vivo models. Extracts showed inhibitory radical scavenging activity against the stable radical 2,2-diphenyl-1-picrylhydrazyl (DPPH) (75%, 43% and 25% of the standard trolox at 1, 10 and 100 mg/ml, respectively; IC50 218 mg/ml). Percentage survival of Saccharomyces cerevisiae cells treated with 10 mM paraquat increased by 21% and 55%, when 1 mg/ml and 10 mg/ml concentrations of the extract, respectively, were added. The cytosolic concentration of TBARS increased in animals treated with paraquat (+283%), while values did not significantly differ from the controls in rats additionally receiving the leaf extract. Paraquat administration also induced a significant increase in hydroperoxide-initiated chemiluminiscence (+76%), that was partially prevented by the leaf extract (+31%). Liver SOD activity was a 158% higher in animals receiving paraquat as compared to the controls. This effect was abolished by administration of the leaf extract. Paraquat administration did not significantly modify the activity of GPx or catalase. Croton cajucara extract increased GPx and catalase activities in paraquat treated-animals by 342% and 70%, respectively. Our results confirm that Croton cajucara leaf extract present radical scavenging activity and reduce oxidative stress induced by paraquat, suggesting the beneficial use as a potential source of antioxidant agents of natural origin.

Low-level laser therapy (LLLT) prevents oxidative stress and reduces fibrosis in rat traumatized Achilles tendon.

BACKGROUND AND OBJECTIVES: The present study investigated the effects of low-level laser therapy (LLLT) on oxidative stress and fibrosis in an experimental model of Achilles tendon injury induced by a single impact trauma. STUDY DESIGN/MATERIALS AND METHODS: Male Wistar rats were randomly divided into four groups (n = 8): control, trauma, trauma+LLLT for 14 days, and trauma+LLLT for 21 days. Achilles tendon traumatism was produced by dropping down a load with an impact kinetic energy of 0.544 J. A low level Ga-As laser was applied with a 904 nm wavelength, 45 mW average power, 5 J/cm(2) dosage, for 35 seconds duration, continuously. Studies were carried out at day 21. RESULTS: Histology showed a loss of normal architecture, with inflammatory reaction, angiogenesis, vasodilatation, and extracellular matrix formation after trauma. This was accompanied by a significant increase in collagen concentration when compared the control group. Oxidative stress, measured by the concentration of thiobarbituric acid reactive substances and hydroperoxyde-initiated chemiluminiscence, was also significantly increased in the trauma group. Administration of LLLT for 14 or 21 days markedly alleviated histological abnormalities reduced collagen concentration and prevented oxidative stress. Superoxide dismutase activity was significantly increased by LLLT treatment over control values. CONCLUSION: LLLT by Ga-As laser reduces histological abnormalities, collagen concentration, and oxidative stress in an experimental model of Achilles tendon injury. Reduction of fibrosis could be mediated by the beneficial effects on the oxidant/antioxidant balance.