Resumo
Purpose: To explore effect and mechanism of olsalazine of Chinese generic drugs on ulcerative colitis induced by dextran sulfate sodium salt (DSS) in BALB/c mice. Methods: The mouse model of ulcerative colitis was induced by free drinking of 3% (w/v) DSS aqueous solution for seven days. The mice were treated with olsalazine (0.6 g·kg-1) of Chinese generic drugs. The therapeutic effect of olsalazine on ulcerative colitis mice was evaluated by measuring disease activity index (DAI), colonic mucosal injury index (CMDI), histopathological score (HS), and detected the expression levels of interleukin (IL)-2, IL-10, tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), IL-1ß in serum and IL-7, IL-17, IL-22, epidermal growth factor (EGF), transforming growth factor ß1 (TGF-ß1) in colonic homogenate of mice. Results: Olsalazine significantly increased the contents of IL-2, IL-10, IL-22, TGF and EGF in ulcerative colitis rats, and significantly decreased the scores of DAI, CMDI, HS and the contents in IL-7, IL-17, TNF-α, IL-1ß and IFN-γ when compared with the model group. It improved the degree of colonic lesion in ulcerative colitis mice. Conclusions: It was suggested that olsalazine has a therapeutic effect on ulcerative colitis induced by DSS in mice, and the mechanism may be related to the increase of IL-2, IL-10, IL-22, TGF, and EGF and the decrease of the expression of IL-7, IL-17, TNF-α, IL-1ß, and IFN-γ.
Assuntos
Animais , Camundongos , Colite Ulcerativa/tratamento farmacológico , Sulfato de Dextrana , Medicamentos GenéricosResumo
Purpose: To examine the effects of a negatively charged nanostructured curcumin microemulsion in experimental ulcerative colitis (UC) in rats. Methods: Four percent acetic acid was used to induce UC. The animals were treated for seven days and randomly assigned to four groups: normal control (NC), colitis/normal saline (COL/NS), colitis/curcumin (COL/CUR), and colitis/mesalazine (COL/MES). The nanostructured curcumin was formulated with a negative zeta potential (-16.70 ± 1.66 mV). Dosage of the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin 1-ß (IL-1ß), interleukin 6 (IL-6), and antioxidant enzymes (catalase, superoxide dismutase, and glutathione peroxidase), macro and microscopic evaluation of the colon tissue were analyzed. Results: The COL/CUR group had a higher level of antioxidant enzymes compared to the COL/MESgroup. The levels of TNF-α, IL-1ß and IL-6 were significantly lower in the colonic tissue of the COL/CUR group rats, when compared to the COL/NS and COL/MES groups (p < 0.001). The presence of ulcers in the colonic mucosa in rats of the COL/NSgroup was significantly higher than in the COL/MES group (p < 0.001). In the NC and COL/CUR groups, there were no ulcers in the colonic mucosa. Conclusions: The nanostructured microemulsion of curcumin, used orally, positively influenced the results of the treatment of UC in rats. The data also suggests that nanostructured curcumin with negative zeta potential is a promising phytopharmaceutical oral delivery system for UC therapy. Further research needs to be done to better understand the mechanisms of the negatively charged nanostructured curcumin microemulsion in UC therapy.
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Animais , Ratos , Colite Ulcerativa , Curcumina , Inflamação , Fitoterapia , MucosaResumo
Purpose: To investigate the effect of givinostat treatment in acetic acid-induced ulcerative colitis model in rats. Methods: Thirty male Wistar albino rats were used. Rats were randomly divided into three equal groups, and colitis was induced on 20 rats by rectal administration of %4 solutions of acetic acid. Twenty rats with colitis were randomly divided into two groups. %0.9 NaCl (saline) solution was administered intraperitoneally to the first group of rats (saline group, n=10) at the dose of 1 mL/kg/day. Givinostat was administered intraperitoneally to the second group rats (Givinostat group, n=10) at the dose of 5 mg/kg/day. Samples were collected for biochemical analysis. Colon was removed for histopathological and biochemical examinations. Results: Plasma tumor necrosis factor-α (TNF-α), pentraxin-3 (PTX-3), and malondialdehyde levels were significantly decreased in the givinostat group compared to the saline group (p<0.05, p<0.001, and p<0.001 respectively; p<0.001, p<0.001, and p<0.001, respectively). Colon TNF-α and prostaglandin F2 alpha (PGF-2) levels were significantly decreased (p<0.05, and p<0.001, respectively). The givinostat group had a significantly lower histologic score than saline group (p<0.001, and p<0.001, respectively). Conclusions: Givinostat, a good protector and regenerator of tissue and an anti-inflammatory agent, may be involved in the treatment of colitis in the future.
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Animais , Ratos , Regeneração , Terapêutica , Colite Ulcerativa , Anti-InflamatóriosResumo
Purpose: To investigate the effects of Periplaneta americana L. on ulcerative colitis (UC) induced by a combination of chronic stress (CS) and 2,4,6-trinitrobenzene sulfonic acid enema (TNBS) in rats. Methods: The experiment UC model with CS was established in rats by a combination of chronic restraint stress, excess failure, improper, and TNBS. The body weight, disease activity index (DAI), colonic mucosal injury index (CMDI), histopathological score (HS) and pro-inflammatory mediators were measured. The content of corticotropin-releasing hormone (CRH) in hypothalamus or adrenocorticotropic hormone (ACTH) and corticosteroids (CORT) in plasma were evaluated by enzyme-linked immunosorbent assay. The proportion of T lymphocyte subsets was detected by flow cytometry, and gut microbiota was detected by 16S rDNA amplicon sequencing. Results: Weight loss, DAI, CMDI, HS and proinflammatory mediators were reversed in rats by P. americana L. treatment after UC with CS. Increased epidermal growth factor (EGF) was observed in P. americana L. groups. In addition, P. americana L. could reduce the content of CRH and ACTH and regulate the ratio of CD3+, CD3+CD8+ and CD3+CD4+CD25+/CD4+ in spleen. Comparably, P. americana L. changes composition of gut microbiota. Conclusions: The ethanol extract of Periplaneta Americana L. improves UC induced by a combination of CS and TNBS in rats.
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Animais , Ratos , Periplaneta , Terapêutica , Colite Ulcerativa , Etanol , Microbioma GastrointestinalResumo
ABSTRACT Purpose: The present study aimed at testing a new formulation of mesalazine linked to chondroitin sulfate and its components alone in the treatment of actinic proctitis in rats. Methods: Forty-seven female Wistar rats were submitted to pelvic radiation and divided into eight groups: control A, mesalazine A, chondroitin A, and conjugate A, gavage of the according substance two weeks after irradiation and sacrifice three weeks after oral treatment; control C, mesalazine C, chondroitin C, and conjugate C, sacrifice six weeks after oral treatment. The rectum was submitted to histological characterization for each of the findings: inflammatory infiltrate, epithelial degeneration, mucosal necrosis, and fibrosis. Results: The inflammatory infiltrate was more intense in chondroitin A, mesalazine A, and conjugate C. The collagen deposition was less intense in chondroitin A, and mesalazine A, and more intense in control C. Conclusions: Mesalazine and chondroitin alone were efficacious in inducing a delayed inflammatory response, hence reducing the late fibrosis. The conjugate was able to induce an ever more delayed inflammatory response.
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Animais , Feminino , Ratos , Proctite/tratamento farmacológico , Colite Ulcerativa/tratamento farmacológico , Reto , Anti-Inflamatórios não Esteroides/uso terapêutico , Administração Oral , Ratos Wistar , Mesalamina/uso terapêuticoResumo
Purpose To study the Periplaneta americana L. extract Ento-B on the treatment of chronic ulcerative colitis induced by 2,4-dinitrochlorobenzene and acetic acid in rats and to explore its primary mechanism of action. Methods Using 2,4-dinitrochlorobenzene combined with acetic acid to induce chronic ulcerative colitis (chronic UC) in rats. The sulfasalazine (400 mg/kg) and Ento-B (200 mg/kg, 100 mg/kg,50 mg/kg) were given by intragastric administration and the effect was evaluated according to the disease activity index (DAI) score, colon mucosal injury index (CMDI) score, histopathological score (HS) and the serum levels of Interleukin-4(IL-4), Interleukin-10(IL-10), Tumor necrosis factor-(TNF-), Malondialdehyde(MDA), Superoxide dismutase(SOD) and Inducible nitric oxide synthase(iNOS.) Results Compared with the model group, all doses of Ento-B could reduce the score of CMDI (p 0.05), HS(p < 0.05 or p < 0.01), significantly increased the expression of IL-4, IL-10, SOD (p < 0.01) and decreased the levels of TNF-alfa, MDA, iNOS in serum of UC rats, significantly improving the degree of colon lesionsin UC rats. Conclusions Ento-B may play an important role in the treatment of ulcerative colitis induced byUC rats. The mechanism may be related to the increased expression of IL-4, IL-10, SOD and reduced expression of TNF-alfa, MDA, iNOS.(AU)
Assuntos
Animais , Ratos , Periplaneta , Dinitroclorobenzeno/administração & dosagem , Ácido Acético/administração & dosagem , Colite Ulcerativa/tratamento farmacológico , Colite Ulcerativa/veterináriaResumo
Purpose: To investigate the mechanism of Periplaneta americana extract promoting intestinal mucosal repair of OXZ-induced colitis in rat. Methods: All experiments used an equal number of male and female SD rats (n=48). We injected OXZ into the colon to induce UC rat model. To determine the optimal concentration of P. Americana's extract (PA-40), it was classified into low (L), medium (M), and high (H) doses. After OXZ treatment, each drug was administered by enema for 7 consecutive days. Rats were divided into the following 6 groups: (1) Saline treatment group (NC), (2) OXZ treatment UC model group (MC), (3) OXZ + budesonide group (BUN), (4) OXZ + PA-40 L group, (5) OXZ + PA-40 M group, (6) OXZ + PA-40 H group. Disease activity index (DAI) scores, colon length, histopathological score, serum cytokine level (IL-4, IL-10, iNOS, tNOS), and amount of MPO, EGF, IL-13 in colonic mucosa were measured. Results: PA treatment had a significant healing effect on the OXZ-colitis model and significantly reduced the lesioned area, especially in the PA-40H groups. PA treatment did not alter the expression of IL-10 and MPO level, but increased EGF (epidermal growth factor) and decrease IL-13 in the colonic tissue. PA inhibited the rise of NOSs (nitric oxide synthase) and decreased the serum IL-4 level. Conclusions: The data suggest that Periplaneta americana extract may be a potential compound for the treatment of colonic lesions. The mechanism may be related to inhibiting the secretion of IL-13 and promoting the formation of EGF.(AU)
Assuntos
Animais , Ratos , Periplaneta , Colite Ulcerativa/terapia , Colite Ulcerativa/veterinária , Mucosa IntestinalResumo
Purpose To examine the therapeutic effect of external adenosine on an acetic acid-induced acute ulcerative colitis model in rats. Methods Thirty male mature rats were divided into three groups as control, acute colitis (AC) and AC+adenosine group (AC+AD). AC was induced by rectal administration of 4% acetic acid (AA). 5mg/kg/day adenosine was performed i.p for 4 weeks to AC+AD group. Rectum and colon were excised for microscopic and histopathological histopathologic evaluations, and immunohistochemical analysis of nuclear factor kappa B (NF-kB). Blood samples were collected for biochemical detection of TNF-α, Pentraxin-3 and malondialdehyde (MDA) levels. Results AC group had generalized hyperemia and hemorrhage with increased macroscopic and histopathological scores compared with control (P <0.0001) while adenosine treatment decreased these scores significantly (P <0.001), with reduced distribution of disrupted epithelium, leukocyte infiltrates, and focal hemorrhage. AC group showed significantly increased immunoexpression of NF-kB in rectum, plasma and tissue levels of TNF-α, plasma Pentraxin-3 and MDA levels (P <0.0001) while adenosine reduced these levels (P < 0.05). Conclusion Adenosine appears to promote healing of colon and rectum exposed to AA-induced AC, suggesting a boosting effect of adenosine on the intestinal immune system to cure ulcerative colitis.(AU)
Assuntos
Animais , Masculino , Ratos , Colite Ulcerativa/tratamento farmacológico , Adenosina/uso terapêutico , NF-kappa B/antagonistas & inibidores , Modelos AnimaisResumo
Background: Colitis murine models have become essential tools to investigate the molecular and cellular mechanisms that lead to infl ammatory bowel disease (IBD), such as ulcerative colitis (UC). DSS-induced colitis model faithfully reproduces many of the clinical presentation and immunological disturbances observed in UC. Notwithstanding mice can show differential susceptibilities and responsiveness to dextran sodium sulfate (DSS), and varying DSS concentration and molecular weights appear to be associated with the severity of inflammation. The aim of this study was to analyze the features of mice induced colitis using different DSS concentrations and molecular weights. Materials, Methods and Results: C57BL/6 mice received 2% of high molecular weight DSS (36 000 - 50 000) in drinking water (HDSS2%) or 5% of the same molecular weight (HDSS5%); other group received 5% of low molecular weight DSS (10 000) (LDSS5%). During the 7 days of DSS administration, animals were observed for weight loss, stool consistency and presence of blood feces to determine the disease activity index (DAI). On day 8, colons were removed, measured and weighed for indirect assessment of infl ammation. The tissue samples were processed for histological analysis and blood samples were collected for hematological analysis. Our results demonstrated that HDSS5% group began to show significant clinical signs starting from day 1, HDSS2% on day 2 and LDSS5% on day 3 (P < 0.05). However, from day 3, HDSS5% group presented DAI significantly higher than other groups (P < 0.001). In addition, DSS administration for 7 days was associated with significant (P < 0.05) changes in mice body weight compared to control animals. Group HDSS2% showed a weight loss of 23.8%±3.0, and HDSS5% and LDSS5% groups, presented weight loss of 32.65%±0.0 and 8.7%±1.7, respectively. From day 6, HDSS5% group presented weight loss significantly greater than HDSS2% and LDSS5% groups (P < 0.05). In colon macroscopic analysis, high molecular weight DSS groups showed a significantly macroscopic colon changes (P = 0.001) and hematological parameters alteration (P < 0.005) compared to control group. In histological features of colitis, these groups presented a higher histological score compared to normal colon (P < 0.001), with crypt damage, mucosal ulceration and cell inflammatory infiltration. Mice from group LDSS5% did not present significant macroscopic colon changes, hematological parameters alteration, and histological score compared to control group. Discussion: Results of the present study evidenced that acute colonic mucosal injury induced by DSS is dependent on the concentration and molecular weight of DSS administered in drinking water, and these findings are important consideration for reproducible induction of experimental colitis with this model. Moreover, DSS with high molecular weight and high concentration can initiate a severe colitis, which may not be an appropriate model for studies of therapeutic regeneration of the colonic mucosa. Thus, identification of differences in mice response to DSS could provide the basis for investigations of susceptibility or resistance to colitis. DSS-induced colitis model study contributes to the understanding of IBD and in the finding for new therapies targeting the reduction of inflammation.
Assuntos
Animais , Masculino , Camundongos , Colite Ulcerativa/induzido quimicamente , Sulfato de Dextrana/efeitos adversosResumo
Background: Histiocytic ulcerative colitis (HUC), also known as granulomatous Boxers colitis or colitis similar to Whipples disease is a condition affecting especially Boxer dogs. The disease is characterized by chronic increase in the defecation frequency, tenesmus, fetid dark-brown stools with blood streaks and mucus. Histopathology of a colorectal biopsy confirms the clinical diagnosis, when infiltrates of markedly PAS-positive macrophages are observed in the colonic lamina propria and submucosa. This communication reports a case of histiocytic ulcerative colitis in a Boxer dog in Brazil. Case: A Boxer dog, with one year and three months of age had been presenting, since it was nine months old, increased frequency of defecation, tenesmus, intermittent diarrhea, loose stools with streaks of liquid blood, and coprophagy; however, no weight loss or appetite loss were noticed. After an initial period of three months experiencing the aforementioned signs, the dog started with persistent diarrhea with bright red blood, mild prostration, weight loss, and voracious appetite. Because of continuous deteriorating condition and treatment refractoriness, the dog was euthanized. At necropsy, the colon was decreased in size with thickened mucosa and foci of ulceration, apart of enlarged mesenteric lymph nodes. Tissue fragments were collected and fixed in 10% formalin, processed following standard procedures for histopathology, and stained with Hematoxylin-Eosin (HE). Selected sections from samples of intestines and mesenteric lymph nodes were also stained with Periodic Acid Shiff (PAS) and Brown-Hopps adapted Gram Staining. Microscopic findings in the colon included infiltration with rounded to oval bulky macrophages, with eccentric nuclei and abundant eosinophilic and slightly granular cytoplasm. These macrophages were distributed in the basal lamina propria and submucosa, and there also was diffuse infiltration of lymphocytes and plasma cells. Extensive multifocal mucosal ulcerations with exposure of the submucosa were also observed. The cytoplasm of macrophages was strongly marked when stained by Periodic Acid Schiff. Macrófagos do cólon e do linfonodo mesentérico não coraram pela técnica de Gram. Discussion: This diagnosis of histiocytic ulcerative colitis was based on the clinical and pathological findings, especially the association of the clinical signs with the infiltrates of markedly PAS-positive macrophages within the colonic lamina propria and submucosa, which is considered a typical characteristic of the condition. The disease afflicts mainly young Boxer dogs, as it was recorded here. In most cases, there is neither weight loss, nor appetite loss, and the hair coat maintains a healthy appearance. However, in chronic cases such this described here, the dogs may show wasting. Ultrastructural and immunohistochemical findings in macrophages of HUC have indicated the participation of Escherichia coli in the etiopathogeny of the disease. The Boxer dogs predisposition to HUC has been attributed to a hereditary abnormality that confers invasion and persistence of an adherent E. coli group. This paper reports the importance of the histiocytic ulcerative colitis as an enteric condition affecting Boxer dogs also in Brazil.
Assuntos
Animais , Cães , Colite Ulcerativa/veterinária , Histiócitos/patologia , Técnicas Histológicas/veterináriaResumo
Background: Histiocytic ulcerative colitis (HUC), also known as granulomatous Boxers colitis or colitis similar to Whipples disease is a condition affecting especially Boxer dogs. The disease is characterized by chronic increase in the defecation frequency, tenesmus, fetid dark-brown stools with blood streaks and mucus. Histopathology of a colorectal biopsy confirms the clinical diagnosis, when infiltrates of markedly PAS-positive macrophages are observed in the colonic lamina propria and submucosa. This communication reports a case of histiocytic ulcerative colitis in a Boxer dog in Brazil. Case: A Boxer dog, with one year and three months of age had been presenting, since it was nine months old, increased frequency of defecation, tenesmus, intermittent diarrhea, loose stools with streaks of liquid blood, and coprophagy; however, no weight loss or appetite loss were noticed. After an initial period of three months experiencing the aforementioned signs, the dog started with persistent diarrhea with bright red blood, mild prostration, weight loss, and voracious appetite. Because of continuous deteriorating condition and treatment refractoriness, the dog was euthanized. At necropsy, the colon was decreased in size with thickened mucosa and foci of ulceration, apart of enlarged mesenteric lymph nodes. Tissue fragments were collected and fixed in 10% formalin, processed following standard procedures for histopathology, and stained with Hematoxylin-Eosin (HE). Selected sections from samples of intestines and mesenteric lymph nodes were also stained with Periodic Acid Shiff (PAS) and Brown-Hopps adapted Gram Staining. Microscopic findings in the colon included infiltration with rounded to oval bulky macrophages, with eccentric nuclei and abundant eosinophilic and slightly granular cytoplasm. These macrophages were distributed in the basal lamina propria and submucosa, and there also was diffuse infiltration of lymphocytes and plasma cells. Extensive multifocal mucosal ulcerations with exposure of the submucosa were also observed. The cytoplasm of macrophages was strongly marked when stained by Periodic Acid Schiff. Macrófagos do cólon e do linfonodo mesentérico não coraram pela técnica de Gram. Discussion: This diagnosis of histiocytic ulcerative colitis was based on the clinical and pathological findings, especially the association of the clinical signs with the infiltrates of markedly PAS-positive macrophages within the colonic lamina propria and submucosa, which is considered a typical characteristic of the condition. The disease afflicts mainly young Boxer dogs, as it was recorded here. In most cases, there is neither weight loss, nor appetite loss, and the hair coat maintains a healthy appearance. However, in chronic cases such this described here, the dogs may show wasting. Ultrastructural and immunohistochemical findings in macrophages of HUC have indicated the participation of Escherichia coli in the etiopathogeny of the disease. The Boxer dogs predisposition to HUC has been attributed to a hereditary abnormality that confers invasion and persistence of an adherent E. coli group. This paper reports the importance of the histiocytic ulcerative colitis as an enteric condition affecting Boxer dogs also in Brazil.(AU)
Assuntos
Animais , Cães , Colite Ulcerativa/veterinária , Histiócitos/patologia , Técnicas Histológicas/veterináriaResumo
PURPOSE: To investigate the effect of enemas containing probiotics and budesonide on the colonic mucosa in experimental colitis. METHODS: Fifty male Wistar rats with experimental colitis induced by 10 percent acetic acid enema were randomized to five groups (10 rats each) according to the treatment: group 1 - saline solution, group 2 - budesonide (0.75 mg/kg/day), group 3 - probiotics (1mg/day), group 4 - probiotics plus budesonide, and group 5 - control, with not-treated rats. The following variables were studied: body weight, macroscopic and microscopic score of the colonic mucosa, and DNA content of the mucosa. RESULTS: All animals lost weight between the beginning and the end of the experiment (280+ 16 mg versus 249+21 mg, p< 0.001). There was no significant difference among the groups in relation to both the macroscopic and histological score. The budesonide + probiotic group showed higher DNA content than control group (1.24+ 0.15 versus 0.92+ 0.30 mg/100mg of tissue, p=0.01). CONCLUSION: Budesonide in addition to probiotics enhance the mucosal trophism in experimental colitis.(AU)
OBJETIVO: Investigar o efeito da administração retal de probióticos e budesonida na mucosa colônica de ratos com colite experimental. MÉTODOS: Cinquenta ratos Wistar com colite experimental induzida pelo ácido acético à 10 por cento foram randomizados em 5 grupos (n=10 por grupo) para diferentes tratamentos: grupo 1 - solução fisiológica; grupo 2 - budesonida (0,75mg/kg/dia); grupo 3 - probióticos (1 g/dia); grupo 4 - probióticos associados a budesonida; e finalmente grupo 5 - controle, composto por ratos sem tratamento. As seguintes variáveis foram estudadas: peso corporal, aspecto macroscópico e microscópico da mucosa e conteúdo de DNA da mucosa colônica. RESULTADOS: Todos os animais perderam peso entre o início e o fim do experimento (280±16 vs 249±21g; p<0.001). Não houve diferença estatística significativa entre os grupos em relação a macroscopia e histologia. O grupo budesonida + probiótico apresentou conteúdo de DNA maior que o grupo controle (1,24±0,15 versus 0,92±0,30 g/100g de tecido; p=0,01). CONCLUSÃO: A associação de budesonida com probióticos acelera o trofismo mucoso na colite experimental.(AU)
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Animais , Masculino , Ratos , Budesonida/uso terapêutico , Colite Ulcerativa/tratamento farmacológico , Anti-Inflamatórios/uso terapêutico , Probióticos/uso terapêutico , Mucosa Intestinal , DNA/genética , Budesonida/administração & dosagem , Colite Ulcerativa/induzido quimicamente , Colite Ulcerativa/genética , Probióticos/administração & dosagem , Mucosa Intestinal/ultraestrutura , Peso Corporal , Ácido Acético , Biópsia , Análise de Variância , Estatísticas não Paramétricas , Enema , Modelos Animais de Doenças , Distribuição Aleatória , Ratos WistarResumo
PURPOSE: The aim of this study was to investigate the effect of enemas containing probiotics and budesonide on the systemic inflammatory response in experimental colitis. METHODS: Fifty male Wistar rats with experimental colitis induced by 10 percent acetic acid enema were randomized to five groups (10 rats each) according to the treatment: group 1 - saline solution, group 2 - budesonide (0.75 mg/kg/day), group 3 - probiotics (1mg/day), group 4 - probiotics plus budesonide, and group 5 - control, with not-treated rats. The following variables were studied: body weight, serum levels of albumin, C-reactive protein and interleucine-6 (IL-6). RESULTS: All animals lost weight between the beginning and the end of the experiment (280+ 16 mg versus 249+21 mg, p< 0.001). There was a significant decrease in the serum albumin between the normal pre-induction level (3.45 + 0.49mg/dL) and the 1st day after colitis induction (1.61+051mg/dL, p< 0.001) in all treated groups when compared to the control group. C- reactive protein increased after induction and diminished on the 7th day in all groups. In the control group there was an increase in the IL-6 after colitis induction. None of the treated groups significantly differed from IL-6 pre-colitis status (p>0.05). Only probiotic rats presented a significant decrease of IL-6 than controls (0,30±0,08 mg/dL vs. 0,19±0,03 mg/dL; p<0.01). CONCLUSION: Probiotic associated with budesonida Probiotics are effective to diminished inflammatory status mediated by IL-6 in experimental colitis.(AU)
OBJETIVO: Investigar o efeito da administração retal de probióticos e budesonida na resposta inflamatória de ratos com colite experimental. MÉTODOS: Cinqüenta ratos Wistar com colite experimental induzida pelo acido acético à 10 por cento foram randomizados em 5 grupos (n=10 por grupo) para diferentes tratamentos: grupo 1 - solução fisiológica; grupo 2 budesonida (0,75mg/kg/dia); grupo 3 - probióticos (1 g/dia); grupo 4 - probióticos associados a budesonida; e finalmente grupo 5 - controle, composto por ratos sem tratamento. As seguintes variáveis foram estudadas: peso corporal, dosagens séricas de albumina, proteína C reativa (PCR) e interleucina-6 (IL-6). RESULTADOS: Todos os animais perderam peso entre o inicio e o fim do experimento (280±16 vs 249±21g; p<0.001). Ocorreu uma queda significativa da albumina sérica entre o normal (3,45±0,49g/dL) e o 1º dia de colite (grupo 5 = 1,61±0,51 g/dL; p <0.001) em todos grupos com tratamento em relação ao grupo controle. A PCR aumentou após a indução da colite, diminuindo no sétimo dia de colite em todos os grupos. No grupo controle houve um aumento da IL-6 após a indução da colite. Nenhum dos grupos de tratamento diferiu significantemente dos valores de IL-6 antes da indução a colite (p>0.05). As comparações entre o grupo controle (0,30±0,08 mg/dL) e outros mostraram que houve uma queda significante nos níveis de IL-6 apenas no grupo probiótico (0,19±0,03 mg/dL; p<0.01). CONCLUSÃO: Probióticos são efetivos na diminuição do estado inflamatório mediado pela IL-6 na colite experimental.(AU)