Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 11 de 11
Filter
Add more filters










Publication year range
1.
Exp Cell Res ; 359(2): 431-440, 2017 10 15.
Article in English | MEDLINE | ID: mdl-28826677

ABSTRACT

Extracellular matrix (ECM) remodeling is necessary for a health adipose tissue (AT) expansion and also has a role during weight loss. We investigate the ECM alteration during weight cycling (WC) in mice and the role of matrix metalloproteinases (MMPs) was assessed using GM6001, an MMP inhibitor, during weight loss (WL). Obesity was induced in mice by a high-fat diet. Obese mice were subject to caloric restriction for WL followed by reintroduction to high-fat diet for weight regain (WR), resulting in a WC protocol. In addition, mice were treated with GM6001 during WL period and the effects were observed after WR. Activity and expression of MMPs was intense during WL. MMP inhibition during WL results in inflammation and collagen content reduction. MMP inhibition during WL period interferes with the period of subsequent expansion of AT resulting in improvements in local inflammation and systemic metabolic alterations induced by obesity. Our results suggest that MMPs inhibition could be an interesting target to improve adipose tissue inflammation during WL and to support weight cyclers.


Subject(s)
Dipeptides/pharmacology , Extracellular Matrix/metabolism , Intra-Abdominal Fat/metabolism , Matrix Metalloproteinase Inhibitors/pharmacology , Obesity/enzymology , Animals , Caloric Restriction , Collagen/genetics , Collagen/metabolism , Diet, High-Fat/adverse effects , Energy Metabolism , Extracellular Matrix/drug effects , Gene Expression , Inflammation/prevention & control , Intra-Abdominal Fat/drug effects , Lipid Metabolism/drug effects , Male , Matrix Metalloproteinase 12/genetics , Matrix Metalloproteinase 12/metabolism , Matrix Metalloproteinase 2/genetics , Matrix Metalloproteinase 2/metabolism , Matrix Metalloproteinase 3/genetics , Matrix Metalloproteinase 3/metabolism , Matrix Metalloproteinase 8/genetics , Matrix Metalloproteinase 8/metabolism , Matrix Metalloproteinase 9/genetics , Matrix Metalloproteinase 9/metabolism , Mice , Obesity/etiology , Obesity/genetics , Obesity/pathology , Protein Isoforms/genetics , Protein Isoforms/metabolism , Weight Gain/drug effects , Weight Loss/drug effects
2.
World J Hepatol ; 7(24): 2551-8, 2015 Oct 28.
Article in English | MEDLINE | ID: mdl-26523207

ABSTRACT

AIM: To study pentoxifylline effects in liver and adipose tissue inflammation in obese mice induced by high-fat diet (HFD). METHODS: Male swiss mice (6-wk old) were fed a high-fat diet (HFD; 60% kcal from fat) or AIN-93 (control diet; 15% kcal from fat) for 12 wk and received pentoxifylline intraperitoneally (100 mg/kg per day) for the last 14 d. Glucose homeostasis was evaluated by measurements of basal glucose blood levels and insulin tolerance test two days before the end of the protocol. Final body weight was assessed. Epididymal adipose tissue was collected and weighted for adiposity evaluation. Liver and adipose tissue biopsies were homogenized in solubilization buffer and cytokines were measured in supernatant by enzyme immunoassay or multiplex kit, respectively. Hepatic histopathologic analyses were performed in sections of paraformaldehyde-fixed, paraffin-embedded liver specimens stained with hematoxylin-eosin by an independent pathologist. Steatosis (macrovesicular and microvesicular), ballooning degeneration and inflammation were histopathologically determined. Triglycerides measurements were performed after lipid extraction in liver tissue. RESULTS: Pentoxifylline treatment reduced microsteatosis and tumor necrosis factor (TNF)-α in liver (156.3 ± 17.2 and 62.6 ± 7.6 pg/mL of TNF-α for non-treated and treated obese mice, respectively; P < 0.05). Serum aspartate aminotransferase levels were also reduced (23.2 ± 6.9 and 12.1 ± 1.6 U/L for non-treated and treated obese mice, respectively; P < 0.05) but had no effect on glucose homeostasis. In obese adipose tissue, pentoxifylline reduced TNF-α (106.1 ± 17.6 and 51.1 ± 9.6 pg/mL for non-treated and treated obese mice, respectively; P < 0.05) and interleukin-6 (340.8 ± 51.3 and 166.6 ± 22.5 pg/mL for non-treated and treated obese mice, respectively; P < 0.05) levels; however, leptin (8.1 ± 0.7 and 23.1 ± 2.9 ng/mL for non-treated and treated lean mice, respectively; P < 0.05) and plasminogen activator inhibitor-1 (600.2 ± 32.3 and 1508.6 ± 210.4 pg/mL for non-treated and treated lean mice, respectively; P < 0.05) levels increased in lean adipose tissue. TNF-α level in the liver of lean mice also increased (29.6 ± 6.6 and 75.4 ± 12.6 pg/mL for non-treated and treated lean mice, respectively; P < 0.05) while triglycerides presented a tendency to reduction. CONCLUSION: Pentoxifylline was beneficial in obese mice improving liver and adipose tissue inflammation. Unexpectedly, pentoxifylline increased pro-inflammatory markers in the liver and adipose tissue of lean mice.

3.
Article in English | LILACS | ID: lil-691770

ABSTRACT

Ibuprofen is widely commercialized in racemic form. Although metabolic chiral inversion occurs through the conversion of R(-)-ibuprofen to S(+)-ibuprofen and the latter enantiomer is considered the active form, clinical trials involving the administration of a racemate to S-enantiomer dosage ratio of 1:0.5 have demonstrated that S(+)-ibuprofen is as efficacious as the racemic formulation. Moreover, the R(-)-enantiomer has been implicated in adverse gastrointestinal effects found with the racemic form, but the mechanisms involved in this process are not yet fully understood. The aim of the present study was to evaluate the anti-inflammatory activity of a racemate to S(+)-ibuprofen dosage ratio of 1:0.5 using the carrageenan air pouch model of inflammation and determine both ulcerogenic activity and the chiral conversion rate in rats. An in vitro study of the cytotoxicity of racemate and S(+)-ibuprofen in gastric cells was also performed. Although the plasma level of S(+)-ibuprofen was raised after racemate administration, no significant difference was found in anti-inflammatory activity, as assessed by exudate formation, PGE2 production and leukocyte migration to the air pouches. Fewer gastric lesions were found after S(+)-ibuprofen administration, despite the low gastric PGE2 content. In the in vitro study, the racemic compound proved more cytotoxic than S(+)-ibuprofen. The present findings suggest that the S-enantiomer of ibuprofen could be considered a therapeutic alternative to minimize gastrointestinal side effects, since the chiral inversion of R(-)-ibuprofen to S(+)-ibuprofen did not result in an improved anti-inflammatory response.


O Ibuprofeno é normalmente comercializado na forma racêmica. Embora ocorra inversão quiral convertendo a forma R(-)- em S(+)-ibuprofeno e, a última seja considerada a forma ativa, a administração da proporção 1:0,5 (racemato: S-enantiômero) demonstrou que o S(+)-ibuprofeno é mais eficaz que a formulação racêmica. Adicionalmente, o R(-)-enantiômero está envolvido nos efeitos adversos gastrintestinais descritos para a formulação racêmica, embora os mecanismos não sejam complemente compreendidos. O objetivo deste estudo foi avaliar a atividade antiinflamatória da proporção 1:0,5 (racemato:S-ibuprofeno) utilizando o modelo experimental de bolsa de ar, a atividade ulcerogênica e a taxa de conversão quiral em ratos. Também estudamos in vitro, a citotoxicidade provocada pelo racemato e S(+)-ibuprofeno em células gástricas. Embora os níveis plasmáticos de S(+)-ibuprofeno tenham aumentado após a administração do racemato, a atividade antiinflamatória avaliada pela formação de exsudato, produção de PGE2 e migração de leucócitos para a bolsa de ar não foram diferentes. As lesões gástricas foram reduzidas após a administração de S(+)-ibuprofeno, apesar da inibição de PGE2 gástrica. In vitro, o composto racêmico foi mais citotóxico que o S(+)-ibuprofeno. Nossos resultados sugerem que o S-enantiômero do ibuprofeno pode ser considerado uma alternativa terapêutica visando a redução dos efeitos colaterais gastrintestinais, visto que a inversão quiral do R(-)- para o S(+)-ibuprofeno não resultou em melhora do efeito antiinflamatório observado.


Subject(s)
Animals , Male , Rats , Dinoprostone , Ibuprofen/administration & dosage , Ibuprofen/therapeutic use , Stomach Ulcer/drug therapy
4.
In Vitro Cell Dev Biol Anim ; 49(6): 473-8, 2013 Jun.
Article in English | MEDLINE | ID: mdl-23708919

ABSTRACT

Macrophages develop into specialized cell types with special functional properties, depending on locally produced stimuli. Adipose tissue macrophages present particular characteristics, such as the M2 cell phenotype, and produce cytokines and chemokines usually produced by M1 cells. Our aim was to study the role of leptin, which is an adipokine produced and released by adipocytes, in the induction of these characteristics in macrophages found in the adipose tissue. Human CD14(+) cells were obtained and maintained in culture with IFN-γ (classical M1 phenotype), IL-4 (alternative M2 phenotype) or leptin for 5 d. Surface marker expression was then analyzed by cytometry. In addition, the release of tumor necrosis factor alpha (TNF-α), interleukin (IL)-6, IL-1ß, IL-10, IL-1ra, MCP-1, MIP-1α, and RANTES was quantified by ELISA after an LPS stimulus, in the culture supernatant. Macrophages exposed to leptin in culture expressed surface markers that were more similar to the M2 phenotype, but they were able to produce TNF-α, IL-6, IL-1ß, IL-1ra, IL-10, MCP-1, and MIP-1α, as observed for M1 cells. Results suggest that leptin strongly contributes to the phenotype observed in macrophages found in adipose tissue.


Subject(s)
Adipocytes/cytology , Adipocytes/metabolism , Leptin/pharmacology , Macrophages/metabolism , Adipocytes/drug effects , Gene Expression Regulation/drug effects , Humans , Interleukin-1/metabolism , Interleukin-10/metabolism , Interleukin-4/metabolism , Interleukin-6/metabolism , Lipopolysaccharide Receptors/metabolism , Macrophages/drug effects , Tumor Necrosis Factor-alpha/metabolism
5.
Scand J Gastroenterol ; 47(8-9): 943-50, 2012 Sep.
Article in English | MEDLINE | ID: mdl-22630819

ABSTRACT

OBJECTIVE: Infliximab is a monoclonal anti-TNF-α antibody that is used therapeutically to treat Crohn's disease (CD). High levels of pro-inflammatory cytokines, especially TNF-α, have been observed in the gastrointestinal tract of CD patients and were associated with alterations in the mesenteric adipose tissue, which also contributed to the high levels of adipokine release. The authors used a rat model of colitis that produces mesenteric adipose tissue alterations that are associated with intestinal inflammation to study the effects that infliximab treatment has on adipokine production, morphological alterations in adipose tissue and intestinal inflammation. MATERIAL AND METHODS: The ability of infliximab to neutralize rat TNF-α was evaluated in vitro using U937 cells. Colitis was induced by repeated intracolonic trinitrobenzene sulfonic acid instillations and was evaluated by macroscopic score, histopathological analysis, myeloperoxidase activity, TNF-α and IL-10 expression as well as iNOS (inducible NO synthase) expression and JNK phosphorylation in colon samples. The alterations in adipose tissue were assessed by TNF-α, IL-10, leptin, adiponectin and resistin levels as well as adipocyte size and peroxisome proliferator-activated receptor (PPAR)-γ expression. RESULTS: Infliximab treatment controlled intestinal inflammation, which reduced lesions and neutrophil infiltration. Inflammatory markers, such as iNOS expression and JNK phosphorylation, were also reduced. In mesenteric adipose tissue, infliximab increased the production of IL-10 and resistin, which was associated with the restoration of adipocyte morphology and PPAR-γ expression. CONCLUSIONS: Our results suggest that infliximab could contribute to the control of intestinal inflammation by modifying adipokine production by mesenteric adipose tissue.


Subject(s)
Adipose Tissue/drug effects , Adipose Tissue/metabolism , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Antibodies, Monoclonal/pharmacology , Colitis/metabolism , Colitis/pathology , Adipose Tissue/pathology , Analysis of Variance , Animals , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Antibodies, Monoclonal/therapeutic use , Cell Survival/drug effects , Colitis/chemically induced , Colitis/drug therapy , Disease Models, Animal , Gene Expression , Humans , Infliximab , Interleukin-10/metabolism , JNK Mitogen-Activated Protein Kinases/drug effects , JNK Mitogen-Activated Protein Kinases/metabolism , Male , Mesentery , Nitric Oxide Synthase Type II/drug effects , Nitric Oxide Synthase Type II/metabolism , PPAR gamma/drug effects , PPAR gamma/genetics , PPAR gamma/metabolism , Peroxidase/metabolism , Phosphorylation , RNA, Messenger/metabolism , Rats , Rats, Wistar , Resistin/metabolism , Trinitrobenzenesulfonic Acid , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/metabolism , Tumor Necrosis Factor-alpha/pharmacology , U937 Cells
6.
Mol Cell Endocrinol ; 361(1-2): 92-8, 2012 Sep 25.
Article in English | MEDLINE | ID: mdl-22480543

ABSTRACT

Immunosuppressant drugs, such as methotrexate, are able to inhibit cytokine production and leukocyte migration to inflammatory foci; therefore, they could modify the establishment of inflammation in adipose tissue during obesity. Thus, we studied the effects of methotrexate in vivo on high-fat diet induced-obesity in mice and in vitro in isolated and co-cultured adipocytes and macrophages. Obese mice treated with methotrexate presented reduced serum levels of TNF-α, insulin and glucose, and an improvement of insulin sensitivity. Adipose tissue from these mice produced less proinflammatory (TNF-α, IL-6, leptin) and more anti-inflammatory adipokines (adiponectin and IL-10) associated with reduced macrophage infiltration and inflammation. Cytokine inhibition was also confirmed in isolated and co-cultured adipocytes and macrophages. Methotrexate presented anti-lipolytic effect in vivo and, in vitro through adenosine release. Drugs that combine anti-lipolytic effect and the ability to control inflammation in adipose tissue could play a role in the control of insulin resistance and other pathologies associated with obesity.


Subject(s)
Inflammation/complications , Inflammation/pathology , Methotrexate/pharmacology , Obesity/complications , Obesity/pathology , 3T3-L1 Cells , Adipocytes/drug effects , Adipocytes/metabolism , Adipocytes/pathology , Adipose Tissue/drug effects , Adipose Tissue/pathology , Adiposity/drug effects , Animals , Body Weight/drug effects , Coculture Techniques , Cytokines/blood , Cytokines/metabolism , Diet, High-Fat , Epididymis/drug effects , Epididymis/metabolism , Epididymis/pathology , Inflammation/metabolism , JNK Mitogen-Activated Protein Kinases/metabolism , Lipolysis/drug effects , Macrophages/drug effects , Macrophages/metabolism , Macrophages/pathology , Male , Mice , Nitric Oxide Synthase Type II/metabolism , Obesity/metabolism , Phosphorylation/drug effects
7.
Dig Dis Sci ; 56(9): 2545-52, 2011 Sep.
Article in English | MEDLINE | ID: mdl-21380759

ABSTRACT

BACKGROUND: Colitis induced by trinitrobenzene sulfonic acid (TNBS) with reactivation is a good experimental model for studying inflammatory bowel disease pathogenesis and appropriate therapeutics. This experimental model allows the induction of colitis relapse and remission periods and the establishment of chronic disease features, such as the mesenteric adipose tissue alterations observed in Crohn's disease. Lymph node activation and the role of perinodal adipose tissue (PAT) have been poorly studied in this model. Thus, a study of the interactions of lymph nodes and PAT could help to elucidate the mechanisms behind IBD pathogenesis. AIMS: The purpose of this study was to examine lymph nodes and PAT alterations during reactivated TNBS-colitis in Wistar rats. METHODS: In this study, the alterations of PAT and lymph node cells during experimental colitis, induced by repeated intracolonic TNBS instillations, were evaluated, focusing on fatty acid and adipocytokine profile analysis and cytokines production, respectively. RESULTS AND CONCLUSION: Fatty acid analysis of PAT reveals an increase of ω-6 polyunsaturated fatty acids during colits, such as linoleic acid, gamma-linolenic acid and arachidonic acid. ω-6 arachidonic acid was not increased in lymph node cells or serum. PAT also produces elevated levels of pro- and anti-inflammatory adipokines during colitis. Lymph node cells release high levels of IFN-γ and TNF-α but not IL-10, characterizing the predominant Th-1 response associated with this disease. Nevertheless, T cells from animals with colitis demonstrated increased IFN-γ production via a COX-2-dependent mechanism after supplementation with ω-6 arachidonic acid, suggesting that PAT modification could contribute to the lymph node cell activation observed during colitis.


Subject(s)
Adipose Tissue/metabolism , Colitis/chemically induced , Lymph Nodes/metabolism , Trinitrobenzenesulfonic Acid/toxicity , Adipokines/metabolism , Animals , Arachidonic Acid , Colitis/metabolism , Cyclooxygenase 2/genetics , Cyclooxygenase 2/metabolism , Gene Expression Regulation , Inflammation/chemically induced , Inflammation/metabolism , Interferon-gamma/genetics , Interferon-gamma/metabolism , Male , Mesentery , Peroxidase/genetics , Peroxidase/metabolism , Proto-Oncogene Proteins c-bcl-2/genetics , Proto-Oncogene Proteins c-bcl-2/metabolism , Rats , Rats, Wistar , bcl-2-Associated X Protein/genetics , bcl-2-Associated X Protein/metabolism
8.
Scand J Gastroenterol ; 45(3): 315-24, 2010 Mar.
Article in English | MEDLINE | ID: mdl-20017653

ABSTRACT

Diversion colitis occurs commonly in the large bowel remnant after diversion of the fecal stream. Several experimental models of colitis have been described, but none examine the inflammatory alterations that can occur in experimentally defunctioned colons. This characterization could be useful in understanding pathophysiological aspects of diversion colitis, and in developing future therapeutic strategies. Thus, we evaluated the temporal inflammatory alterations in the defunctioned colon of rats by analyzing the histological results, infiltrating neutrophils, pro-inflammatory markers such as cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS), and DNA damage in isolated colonocytes. We compared the obtained data with those from hapten-induced colitis. The experimental diversion of the colon fecal stream induces diversion colitis characterized by an early inflammatory process with increased neutrophil infiltrate, and COX-2 and iNOS expression that resembles, in some aspects, the inflammatory characteristics of chemically induced colitis. After acute inflammation resolution, there was an increase in COX-2 and iNOS expression and the presence of lymphoid follicular hyperplasia and ulcerations, suggesting that diversion colitis can be experimentally established and useful for studying different pathophysiological aspects of this condition.


Subject(s)
Colitis/pathology , Colitis/physiopathology , Inflammation/physiopathology , Animals , Colitis/chemically induced , Cyclooxygenase 2/metabolism , Disease Models, Animal , Male , Nitric Oxide Synthase/metabolism , Rats , Rats, Wistar
9.
Pharmacol Res ; 60(4): 341-6, 2009 Oct.
Article in English | MEDLINE | ID: mdl-19450685

ABSTRACT

Mesenteric white adipose tissue hypertrophy and modifications in adipocytokine production are described features of Crohn's disease. Experimentally, mesenteric white adipose tissue alterations, associated with intestinal inflammation, can be induced in a model of reactivated colitis by repeated administration of intrarectal trinitrobenzenosulfonic acid (TNBS) in ethanol solution. Crohn's disease patients refractory to corticosteroid treatment are frequently treated with methotrexate; however, there is no information regarding the drug's effect on adipose tissue alterations and in a reactivated colitis experimental model. Thus, we evaluated the effect of methotrexate upon mesenteric WAT alterations and inflammatory features in experimental colitis in rats. Colitis status was evaluated by macroscopic score, histopathological analysis, myeloperoxidase activity, TNF-alpha and IL-10 expression, as well as iNOS and TLR-4 expression in colon samples. The adipose tissue alterations were assessed by TNF-alpha, IL-10, leptin and adiponectin production, as well as by macrophage infiltration evaluation. Methotrexate exerts an anti-inflammatory activity in experimental reactivated colitis by regulating the shift from Th1 to Th2 cytokines, reducing TNF-alpha and improving IL-10 production. Additionally, methotrexate reduces other inflammatory parameters in the colon, such as iNOS and TLR-4 expression. In mesenteric white adipose tissue, methotrexate treatment reduces the production of pro- and anti-inflammatory adipocytokines as well as macrophage infiltration, suggesting that immunosuppressant drugs diminish adipose tissue inflammatory alterations associated with intestinal inflammation.


Subject(s)
Adipose Tissue/drug effects , Colitis/drug therapy , Immunosuppressive Agents/therapeutic use , Intestines/drug effects , Methotrexate/therapeutic use , Adipose Tissue/immunology , Adipose Tissue/pathology , Animals , Cell Movement , Colitis/chemically induced , Cytokines/immunology , Intestines/immunology , Intestines/pathology , Macrophages/cytology , Male , Rats , Rats, Wistar
10.
Int Immunopharmacol ; 9(4): 396-402, 2009 Apr.
Article in English | MEDLINE | ID: mdl-19168155

ABSTRACT

Current knowledge suggests that adipose tissue is an active organ, participating in intestinal and mesenteric disease. Additionally, adipose tissue surrounds the lymph nodes and has special properties, acting as a paracrine regulator of adjacent lymphoid tissues. These adipose tissue depots can express and secrete numerous cytokines, known as adipocytokines, which then modify the action of insulin in adipose tissue itself. Using a well-accepted model of intestinal inflammation, we studied insulin signaling in mesenteric adipose tissue (MAT) and in perinodal mesenteric adipose tissue (PAT). Our results showed that the action of insulin is modified during the intestinal inflammatory response in these adipose tissue depots. MAT became resistant to insulin signaling, as evaluated by the IRS/AKT pathway, in the inflammation. This resistant status was associated with high JNK activity and the presence of infiltrating macrophages. Conversely, the adipose tissue that involves the mesenteric lymph nodes acquired greater sensitivity to insulin signaling via IRS/AKT, probably via up-regulation of IRS during experimental colitis. We demonstrated experimentally the existence of site-specific adaptive alterations in two mesenteric adipose tissue depots to the intestinal inflammatory response, probably resulting in alterations in free fatty acids and other secretory products supplied by the adjacent tissues that could act as inflammatory modulator substances.


Subject(s)
Adipose Tissue/metabolism , Colitis/metabolism , Insulin Receptor Substrate Proteins/metabolism , Intestinal Mucosa/metabolism , Adipose Tissue/drug effects , Adipose Tissue/immunology , Animals , Colitis/chemically induced , Colitis/immunology , Insulin/pharmacology , Insulin Receptor Substrate Proteins/drug effects , Intestines/immunology , Male , Mesentery/immunology , Mesentery/metabolism , Peroxidase/metabolism , Phosphorylation/drug effects , Phosphorylation/physiology , Rats , Rats, Wistar , Signal Transduction/physiology , Trinitrobenzenesulfonic Acid/pharmacology , Tyrosine/drug effects , Tyrosine/metabolism
11.
Phytother Res ; 23(3): 324-9, 2009 Mar.
Article in English | MEDLINE | ID: mdl-18979524

ABSTRACT

Inflammatory bowel disease (IBD), Crohn's disease and ulcerative colitis are chronic enteropathies that probably result from a dysregulated mucosal immune response. These pathologies are characterized by oxidative and nitrosative stress, leukocyte infiltration and up-regulation of pro-inflammatory substances. Current IBD treatment presents limitations in both efficacy and safety that stimulated the search for new active compounds. Garcinia cambogia extract has attracted interest due to its pharmacological properties, including gastroprotective effects. In this study, the antiinflammatory activity of a garcinia extract was assessed in TNBS-induced colitis rats. The results obtained revealed that garcinia administration to colitic rats significantly improved the macroscopic damage and caused substantial reductions in increases in MPO activity, COX-2 and iNOS expression. In addition, garcinia extract treatment was able to reduce PGE(2) and IL-1beta colonic levels. These antiinflammatory actions could be related to a reduction in DNA damage in isolated colonocytes, observed with the comet assay. Finally, garcinia extract caused neither mortality nor toxicity signals after oral administration. As such, the antiinflammatory effects provided by the Garcinia cambogia extract result in an improvement of several parameters analysed in experimental colitis and could provide a source for the search for new antiinflammatory compounds useful in IBD treatment.


Subject(s)
Anti-Inflammatory Agents/pharmacology , Colitis/drug therapy , Garcinia cambogia/chemistry , Plant Extracts/pharmacology , Animals , Colitis/chemically induced , Colon/metabolism , Colon/pathology , DNA Damage , Dinoprostone/metabolism , Disease Models, Animal , Female , Inflammation Mediators/metabolism , Male , Peroxidase/metabolism , Rats , Rats, Wistar , Trinitrobenzenesulfonic Acid/pharmacology
SELECTION OF CITATIONS
SEARCH DETAIL
...