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Arbutin is utilized in traditional remedies to cure numerous syndromes because of its anti-microbial, antioxidant, and anti-inflammatory properties. This study aimed to evaluate chemopreventive effects of arbutin on azoxymethane (AOM)-induced colon aberrant crypt foci (ACF) in rats. Five groups of rats were used: normal control group (rats injected hypodermically with sterile phosphate-buffered saline once per week for two weeks) and groups 2-5, which were subcutaneously inoculated with 15 mg/kg AOM once a week for two weeks. AOM control and 5-fluorouracil (5-FU) control groups were fed 10% Tween orally daily for 8 weeks using a feeding tube. The treated groups were fed 30 and 60 mg/kg arbutin every day for 2 months. ACF from the AOM control group had aberrant nuclei in addition to multilayered cells and an absence of goblet cells. The negative control group displayed spherical cells and nuclei in basal positions. Histological examination revealed a reduced number of AFC cells from colon tissues of the 5-FU reference group. Arbutin-fed animals showed down-regulation of proliferating cell nuclear antigen (PCNA) and up-regulation of Bax protein compared to AOM control. Rats fed with arbutin displayed a significant increase of superoxide dismutase (SOD) and catalase (CAT) activities in colon tissue homogenates compared to the AOM control group. In conclusion, arbutin showed therapeutic effects against colorectal cancer, explained by its ability to significantly decrease ACF, down-regulate PCNA protein, and up-regulate Bax protein. In addition, arbutin significantly increased SOD and CAT, and decreased malondialdehyde (MDA) levels, which might be due to its anti-proliferative and antioxidant properties.

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Tissue inhibitor of metalloproteinase-2 (TIMP-2) and membrane-type 1-matrix metalloproteinase (MT1-MMP) are always expressed during the cancer process. The aim was to identify which regions of the colon mucosa MT1-MMP and TIMP-2 begin to express themselves, as well as to establish their expression in relation to cell proliferation and mucin production. After intraperitoneal injection of 15 mg/kg of azoxymethane (AOM) at 4, 12, and 20 weeks, histological sections of the middle segment of the rat colon mucosa were evaluated by immunohistochemistry for cell proliferation and expression of MT1-MMP and TIMP-2 and histochemistry for mucin. As a result, a single dose of AOM initially increased the intensity of MT1-MMP and TIMP-2 expression in the conjunctive cells and glands, concurrently with alterations in the distribution of the mucin produced in the gland of the large intestine mucosa and cell proliferation. As a result, at 4 and 12 weeks, a single dose of AOM initially stimulated the expression of MT1-MMP and TIMP-2 in the conjunctive cells and glands with greater intensity. Changes in the cell proliferation and distribution of the mucin produced in the large intestine mucosa gland were observed. We conclude that MT1-MMP and TIMP-2 were first and strongly expressed in all cells of the colon glands, concurrently with an increase in cell proliferation and a diffuse dispersion of mucin, indicating the onset of the dysplasia process following a single dosage of AOM.

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Purpose: The aim of this study was to assess the effects of resistance and aerobic exercise on colorectal cancer (CRC) development in mice induced by azoxymethane (AOM) coupled with colitis. Methods: Forty animals induced with CRC were used, divided into five groups of eight animals each: sedentary; continuous aerobics; continuous anaerobic; aerobic PI; and anaerobic PI. AOM was administered to the animals in two doses of 10 mg/kg each over the course of two weeks, the first dose administered in the third week and the second administered in the fourth. For the colitis, three cycles of dextran sodium sulfate were administered for five days, separated by two weeks of water. The 14th week of the experiment saw the euthanasia, the removal of their colons, and the creation of microscopy slides for histological analysis. Results: Preneoplastic lesions developed in all five groups; there were no significant differences between them. However, in terms of inflammatory symptoms, mucosal ulceration was much more frequently in the exercise groups than in the sedentary group (p = 0.016). The number of polyps overall (p = 0.002), the distal region's polyp development (p = 0.003), and the proximal region's polyp development (p = 0.04) were all statistically different than sedentary group. Conclusions: The study discovered no significant difference in disease activity index scores between groups, but there was a significant difference in the number of polyps and the presence of mucosal ulceration in the colon.

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Melastoma malabathricum (M. malabathricum) extracts have been reported to exert various pharmacological activities including antioxidants, anti-inflammatory and antiproliferative activities. The objective of the present study was to determine the anticarcinogenic activity of its methanol extract (MEMM) against the azoxymethane (AOM)-induced early colon carcinogenesis in rats. Rats were randomly assigned to five groups (n=6) namely normal control, negative control, and treatment (50, 250 or 500 mg/kg of MEMM) groups. Colon tissues were harvested for histopathological analysis and endogenous antioxidant system determination. MEMM was also subjected to HPLC analysis. Findings showed that MEMM significantly (p<0.05) reversed the AOM-induced carcinogenicity by: i) reducing the formation of aberrant crypt foci (ACF) in colon tissues, and; ii) enhancing the endogenous antioxidant activity (catalase, superoxide dismutase and glutathione peroxidase). Moreover, various phenolics has been identified in MEMM. In conclusion, MEMM exerts the in vivo anticarcinogenic activity via the activation of endogenous antioxidant system and synergistic action of phenolics.

Se ha informado que los extractos de Melastoma malabathricum (M. malabathricum) ejercen diversas actividades farmacológicas, incluidas actividades antioxidantes, antiinflamatorias y antiproliferativas. El objetivo del presente estudio fue determinar la actividad anticancerígena de su extracto de metanol (MEMM) contra la carcinogénesis de colon temprana inducida por azoximetano (AOM) en ratas. Las ratas se asignaron al azar a cinco grupos (n=6), a saber, los grupos de control normal, control negativo y tratamiento (50, 250 o 500 mg/kg de MEMM). Tejidos de colon fueron recolectados para análisis histopatológico y determinación del sistema antioxidante endógeno. MEMM también se sometió a análisis de HPLC. Los hallazgos mostraron que MEMM invirtió significativamente (p<0.05) la carcinogenicidad inducida por AOM al: i) reducir la formación de focos de criptas aberrantes (ACF) en los tejidos del colon, y; ii) potenciar la actividad antioxidante endógena (catalasa, superóxido dismutasa y glutatión peroxidasa). Además, se han identificado varios fenólicos en MEMM. En conclusión, MEMM ejerce la actividad anticancerígena in vivo mediante la activación del sistema antioxidante endógeno y la acción sinérgica de los fenólicos.

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Sheep dairy products containing prebiotic and probiotic ingredients may have health-promoting properties. Thus, this study evaluated the effects of sheep milk ice cream [conventional full-fat (CONV), full-fat enriched with probiotic (PROB, 100 mg % wt/wt of Lacticaseibacillus casei 01), or nonfat synbiotic (SYNB, Lacticaseibacillus casei 01 and inulin, 10% wt/wt)] on carcinogen-induced colonic crypt cytotoxicity and premalignant lesion development. Male Swiss mice received 2 doses of colon carcinogen azoxymethane (AOM, 15 mg/kg of body weight) at wk 3 and 4. Two weeks before and during AOM administrations (4 wk) mice were treated with CONV, PROB, or SYNB by gavage (10 mL/kg). Mice were euthanized at wk 4 or 25 (n = 5 or 10 mice/group, respectively). At wk 4, a significant reduction in micronucleated colonocytes was observed in PROB and SYNB groups, and a significant decrease in both p53 expression and apoptosis indexes in colonic crypts was observed in SYNB group. At wk 25, both PROB and SYNB interventions reduced the mean number of colonic premalignant lesions. However, only SYNB group showed lower incidence and number of high-grade premalignant lesions in the colonic mucosa. These findings indicate that PROB or SYNB sheep milk ice cream, especially SYNB intervention, can reduce chemically induced mouse colon carcinogenesis.

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Purpose:To evaluate red propolis, gum arabic and L-lysine activity on colorectal preneoplastic lesions induced by azoxymethane (AOM).Methods:The study featured 4 control groups (I-IV) and 4 experimental groups (V-VIII), totaling 48 rats. Once a week for 2 weeks, animals on control groups received saline, while animals in experimental groups received azoxymethane (15 mg/kg i.p.). The follow up along 16 weeks included daily oral gavage to administer water (I and V), L-lysine (150 mg/kg)(II and VI), própolis (100mg/5ml/kg)(III and VII), or gum arabic (5ml/kg)(IV and VIII). Was performed surgery on the animals in the end of this time in order to collect blood for biological assays (TBARS, GSH), followed by their sacrifice to tissue extract.Results:Oxidative stress (TBARS) and the number of aberrant crypt foci (ACF) in distal colon were lower using própolis (p<0.01 for both parameters). Gum arabic reduced preneoplastic lesions (ACF ≤ 4 crypts) on distal colon and on the entire colon (p<0.05).Conclusions:Red propolis reduced AOM-induced oxidative stress (TBARS) and total number of ACF in the distal colon. L-lysine neither protected against nor enhanced AOM-induced ACF. Gum arabic reduced the number of ACF.(AU)

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Abstract Purpose: To evaluate red propolis, gum arabic and L-lysine activity on colorectal preneoplastic lesions induced by azoxymethane (AOM). Methods: The study featured 4 control groups (I-IV) and 4 experimental groups (V-VIII), totaling 48 rats. Once a week for 2 weeks, animals on control groups received saline, while animals in experimental groups received azoxymethane (15 mg/kg i.p.). The follow up along 16 weeks included daily oral gavage to administer water (I and V), L-lysine (150 mg/kg)(II and VI), própolis (100mg/5ml/kg)(III and VII), or gum arabic (5ml/kg)(IV and VIII). Was performed surgery on the animals in the end of this time in order to collect blood for biological assays (TBARS, GSH), followed by their sacrifice to tissue extract. Results: Oxidative stress (TBARS) and the number of aberrant crypt foci (ACF) in distal colon were lower using própolis (p<0.01 for both parameters). Gum arabic reduced preneoplastic lesions (ACF ≤ 4 crypts) on distal colon and on the entire colon (p<0.05). Conclusions: Red propolis reduced AOM-induced oxidative stress (TBARS) and total number of ACF in the distal colon. L-lysine neither protected against nor enhanced AOM-induced ACF. Gum arabic reduced the number of ACF.

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Moringa (Moringa oleifera) is a plant that has generated great interest in recent years because of its attributed medicinal properties. The aim of this study was to characterize the bioactive compounds of moringa leaves (MO) and evaluate their effect on a colorectal carcinogenesis model. Twenty-four male CD-1 mice were divided into 4 groups: Group 1 fed with basal diet (negative control/NC); Group 2 received AOM/DSS (positive control); Groups 3 and 4 were fed with basal diet supplemented with moringa leaves (2.5% w/w and 5% w/w, respectively) for 12weeks. Moringa leaves exhibited a high content of dietary fiber (~18.75%) and insoluble dietary fiber (2.29%). There were identified 9 phenolic compounds whereas the chlorogenic and ρ-coumaric acid showed the higher contents (44.23-63.34µg/g and 180.45-707.42µg/g, respectively). Moringa leaves decreased the activity of harmful fecal enzymes (ß-glucosidase, ß-glucuronidase, tryptophanase and urease up to 40%, 43%, 103% and 266%, respectively) as well tumors incidence in male CD1-mice (~50% with 5% w/v of moringa dose). These findings suggest that the bioactive compounds of moringa such as total dietary fiber and phenolic compounds may have chemopreventive capacity. This is the first study of the suppressive effect of moringa leaves in an in vivo model of AOM/DSS-induced colorectal carcinogenesis.

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Hepatic encephalopathy (HE) represents a serious complication of acute liver failure (ALF) in which cerebral edema leading to brainstem herniation as a result of increased intracranial hypertension is a major consequence. Long non-coding RNAs (lncRNAs) play a significant role in coordinating gene expression, with recent studies indicating an influence in the pathogenesis of several diseases. To investigate their involvement in the cerebral pathophysiology of ALF, we profiled the expression of lncRNAs in the frontal cortex of mice at coma stage following treatment with the hepatotoxin azoxymethane. Of the 35,923 lncRNAs profiled using microarrays, 868 transcripts were found to be differentially expressed in the ALF-treated group compared to the sham control group. Of these, 382 lncRNAs were upregulated and 486 lncRNAs downregulated. Pathway analysis revealed these lncRNAs target a number of biological and molecular pathways that include cytokine-cytokine receptor interaction, the mitogen activated protein kinase signaling pathway, the insulin signaling pathway, and the nuclear factor-κB signaling pathway. False discovery rate adjustment identified 9 upregulated lncRNAs, 2 of which are associated with neuroepithelial transforming gene 1 (NET1) and the monocarboxylate transporter 2 (Slc16a7), potential contributors to astrocyte cytoskeletal disruption/swelling and lactate production, respectively. Our findings suggest an important role for lncRNAs in the brain in ALF in relation to inflammation, neuropathology, and in terms of the functional basis of HE. Further work on these non-coding RNAs may lead to new therapeutic approaches for the treatment and management of cerebral dysfunction resulting from this potentially life-threatening disorder.

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Colorectal cancer is the fourth worldwide cause of death and even if some dietary habits are consider risk factors, the contribution of food additives including foodgrade titanium dioxide (TiO2), designated as E171, has been poorly investigated. We hypothesized that oral E171 intake could have impact on the enhancement of colorectal tumor formation and we aimed to investigate if E171 administration could enhance tumor formation in a colitis associated cancer (CAC) model. BALB/c male mice were grouped as follows: a) control, b) E171, c) CAC and d) CAC + E171 group (n = 6). E171 used in this study formed agglomerates of 300 nm in water. E171 intragastric administration (5 mg/kg body weight/5 days/10 weeks) was unable to induce tumor formation but dysplastic alterations were observed in the distal colon but enhanced the tumor formation in distal colon (CAC + E171 group) measured by tumor progression markers. Some E171 particles were internalized in colonic cells of the E171 and CAC + E171 groups and both groups showed a decrease in goblet cells in the distal colon. However the CAC + E171 group showed a higher decrease of these cells that act as protection barrier in colon. These results suggest that E171 could worsen pre-existent intestinal diseases.

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The induced colorectal carcinogenesis in rodents has a long history and currently uses the substances 1,2-dimethylhydrazine and azoxymethane. Objective: The aim of this study was to compare the inductive effect of the substances azoxymethane and 1,2-dimethylhydrazine in colorectal carcinogenesis. Method: 30 randomly chosen male Wistar rats were divided into four groups. G1 group was treated with 1,2-dimethylhydrazine and C1 was its control group; G2 group was treated azoxymethane and C2 was its control group. The animals were weekly weighed until euthanasia, when their intestines were removed, processed and analyzed by an experienced pathologist. Results: Among the control groups (C1 and C2) no histologic changes were observed; moderate dysplasia was detected in G2 group; hyperplasia, mild dysplasia, severe dysplasia and carcinoma were observed in G1 group. When this study compared the cost of the substances, 1,2-dimethylhydrazine was more than 50 times less expensive than azoxymethane. Conclusion: Azoxymethane is able to promote histological changes consistent with colorectal carcinogenesis. 1,2-Dimethylhydrazine produced neoplasia and dysplasia, and, compared to the azoxymethane, was more efficient in the induction of colorectal cancer. (AU)

A carcinogênese colorretal induzida em roedores tem longa história e utiliza, atualmente, as substâncias 1,2 dimetil-hidrazina (DMH) e azoximetano (AOM). Objetivo: Comparar o efeito indutivo das substâncias AOM e DMH para o câncer colorretal (CCR). Método: 30 ratos Wistar machos foram randomizados em quatro grupos. O grupo G1 foi inoculado com DMH, o grupo C1 foi seu controle; G2 recebeu o AOM e C2 foi seu controle. Os animais foram pesados semanalmente até a eutanásia, quando tiveram seus intestinos retirados, processados e analisados por um patologista experiente. Resultados: Os animais dos grupos de controle apresentaram tecido colorretal normal e os animais do grupo G2 apresentaram um padrão de displasia moderada. Nas lâminas do grupo G1, foram encontradas regiões de hiperplasia, displasia leve, displasia grave, e carcinoma. Comparado o custo das substâncias AOM e DMH, este último teve um preço mais de 50 vezes menor ao do AOM. Conclusão: AOM é capaz de promover alterações histológicas compatíveis com a carcinogênese colorretal. DMH produziu neoplasia e displasia grave e, comparada ao AOM, foi mais eficiente na indução do câncer colorretal. (AU)

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PURPOSE: To assess weight changes in rats fed diets with different ratios of omegas 3, 6 and 9 submitted to colonic carcinogenesis induced by Azoxymethane (AOM). METHODS: Sixty rats with three weeks of life were distributed into five groups of specific diets containing 12 animals each: GI- Standard diet without adminstration of AOM, GII- Standard diet with adminstration of AOM; GIII- Hyperlipidic diet with adminstration of AOM; GIV-Normolipidic diet with adminstration of AOM; GV- Hypolipidic diet with adminstration of AOM. The weight and food intake of each group were assessed four times in each week throughout the experiment until euthanasia at 36th week. RESULTS: GI and GII had no significant difference in weight. GI showed a significant increase when compared to GIII, GIV and GV. GII also showed a significant increase when compared to GIII, GIV and GV. When comparing intake of GI as compared to GII no significant difference was found, however such groups had higher intake than groups III, IV and V. There were found no difference in weight when comparing amoung rats with and without cancer within each groups: GII, GIII, GIV and GV. CONCLUSIONS: Diets rich in omega 3, 6 and 9 reduced food intake and weight. Rats with colorectal cancer had no decrease in weight as compared to those without this condition in the same group.(AU)

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PURPOSE: To assess weight changes in rats fed diets with different ratios of omegas 3, 6 and 9 submitted to colonic carcinogenesis induced by Azoxymethane (AOM). METHODS: Sixty rats with three weeks of life were distributed into five groups of specific diets containing 12 animals each: GI- Standard diet without adminstration of AOM, GII- Standard diet with adminstration of AOM; GIII- Hyperlipidic diet with adminstration of AOM; GIV-Normolipidic diet with adminstration of AOM; GV- Hypolipidic diet with adminstration of AOM. The weight and food intake of each group were assessed four times in each week throughout the experiment until euthanasia at 36th week. RESULTS: GI and GII had no significant difference in weight. GI showed a significant increase when compared to GIII, GIV and GV. GII also showed a significant increase when compared to GIII, GIV and GV. When comparing intake of GI as compared to GII no significant difference was found, however such groups had higher intake than groups III, IV and V. There were found no difference in weight when comparing amoung rats with and without cancer within each groups: GII, GIII, GIV and GV. CONCLUSIONS: Diets rich in omega 3, 6 and 9 reduced food intake and weight. Rats with colorectal cancer had no decrease in weight as compared to those without this condition in the same group.

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OBJETIVO: Avaliar as repercussões hepáticas da carcinogênese colônica induzida por diferentes doses e tempos de exposição ao azoximetano em ratos Wistar. MÉTODOS: Quarenta e quatro ratos foram distribuídos em quatro grupos. Os animais tinham oito semanas no início do experimento. No grupo 1, receberam 1.0mL de solução salina intraperitonealmente uma vez por semana por duas semanas. No grupo 2, receberam 15 mg/kg de azoximetano intraperitonealmente uma vez por semana por duas semanas. Esses animais foram mortos na 15ª semana do experimento. Os animais do grupo 3 receberam solução salina intraperitonealmente uma vez por semana por duas semanas. Os animais do grupo 4 receberam 20mg/kg de azoximetano intraperitonealmente uma vez por semana por duas semanas. Esses animais foram mortos na 26ª semana do experimento. Os fragmentos de tecido hepático foram corados pela hematoxilina e eosina e avaliadas microscopicamente. RESULTADOS: Grupo 1 e grupo 2 diferiram significantemente em relação a esteatose, mas não houve diferença entre o grupo 3 e o grupo 4. No entanto, no grupo 4 foram observadas lesões pré-neoplásicas (focos de células alteradas, claras, vacuoladas, basofílicas, anfofílicas, tigróides, oncocíticas, pequenas ou acidófilas, espongioses e pelioses) e lesões neoplásicas (colangiomas e adenomas) contendo hepatócitos atípicos de permeio, não identificados no grupo 3. CONCLUSÃO: No modelo de carcinogênese colorretal, lesões hepáticas pré-neoplásicas e neoplásicas aparecem e evoluem na proporção do tempo e dose de exposição ao azoximetano.

OBJECTIVE: To evaluate the hepatic effects of colonic carcinogenesis induced by azoxymethane at different doses and times of exposure in rats. METHODS: Forty-four Wistar rats were divided into four groups. The animals were eight weeks at the beginning of the experiment. group 1 received 1.0ml of saline intraperitoneally once a week for two weeks. Group 2 received 15 mg/kg of azoxymethane intraperitoneally once a week for two weeks. These animals were killed at the 15th week of the experiment. The animals of group 3 received saline intraperitoneally once a week for two weeks. Group 4 animals received 20mg/kg of azoxymethane intraperitoneally once a week for two weeks. These animals were killed at the 26th week of the experiment. The fragments of liver tissue were stained with hematoxylin and eosin and evaluated microscopically. RESULTS: Groups 1 and 2 differed significantly in relation to steatosis, no difference having been found between group 3 and group 4. However, in group 4 we observed pre-neoplastic lesions (foci of altered, clear, vacuolated, basophilic, amphophilic tigroid, oncocytic, small or acidophilus cells, spongiosis and peliosis) and neoplastic lesions (adenomas and colangiomas) containing atypical hepatocytes in between, not identified in group 3. CONCLUSION: In the model of colorectal carcinogenesis, preneoplastic and neoplastic hepatic lesions appear and evolve in proportion to the time of exposure and dose of azoxymethane.

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PURPOSE: To determine whether a hypercaloric and hyperlipidic diet enriched with polyunsaturated fatty acids influences the formation of aberrant crypt foci (ACF) in colonic mucosa of Wistar rats treated with azoxymethane (AOM). METHODS: At eight weeks of life, the rats were assigned to four groups: Group I―standard diet (STD) not treated with AOM; Group II―hypercaloric and hyperlipidic diet (FED), not treated with AOM; Group III―STD, treated with AOM; Group IV―FED, treated with AOM. At 16 weeks, the animals were injected intraperitoneal with 0.9 percent saline solution (Group I and II) or AOM at 15mg/Kg (Groups III and IV) once a week for two weeks. Fifteen weeks later, the animals were euthanized. RESULTS: FED promoted weight gain in Groups II and IV compared to Groups I and III, respectively. The groups did not differ with regard to the total number of ACF. The Chi-square test revealed no predominance of the presence of foci with <4 crypts. However, foci with ≥5 crypts were proportionally more prevalent in Group III than in Group IV (p=0.043). CONCLUSION: The administration of polyunsaturated fatty acids did not interfere with the formation of aberrant crypt foci, but reduced ACF multiplicity, exercising an attenuating effect on carcinogenesis.(AU)

OBJETIVO: Determinar se uma dieta hipercalórica, hiperlipídica, rica em ácidos graxos poliinsaturados (FED) tem influência na formação de focos de cripta aberrante (FCA) em mucosa cólica de ratos Wistar expostos ao azoximetano (AOM). MÉTODOS: Com oito semanas de vida, os ratos foram distribuídos em quatro grupos: Grupo I: Dieta padrão (SD) sem AOM; Grupo II: FED, sem AOM; Grupo III: SD, com AOM; Grupo IV: FED com AOM. Com 16 semanas, os animais dos grupos I e II receberam injeções intraperitoneais de solução salina 0,9 por cento, enquanto os dos grupos III e IV receberam AOM na dose de 15mg/Kg de peso, 1 vez por semana por duas semanas. Quinze semanas após, os animais foram mortos. RESULTADOS: FED promoveu aumento de peso nos grupos II e IV em relação aos grupos I e III. Não houve aumento significante no número total de FCA entre os grupos. Em relação à multiplicidade das criptas por FCA, o teste do qui-quadrado mostrou que não houve predominância da presença <4 criptas por foco. Contudo, focos ≥5 criptas foram proporcionalmente mais prevalentes no grupo III que no grupo IV (p=0,043). CONCLUSÃO: Os ácidos graxos poliinsaturados não interferem na formação de focos de cripta aberrante, contudo reduz sua multiplicidade, exercendo efeito atenuador na carcinogênese.(AU)

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PURPOSE: To determine whether a hypercaloric and hyperlipidic diet enriched with polyunsaturated fatty acids influences the formation of aberrant crypt foci (ACF) in colonic mucosa of Wistar rats treated with azoxymethane (AOM). METHODS: At eight weeks of life, the rats were assigned to four groups: Group I―standard diet (STD) not treated with AOM; Group II―hypercaloric and hyperlipidic diet (FED), not treated with AOM; Group III―STD, treated with AOM; Group IV―FED, treated with AOM. At 16 weeks, the animals were injected intraperitoneal with 0.9 percent saline solution (Group I and II) or AOM at 15mg/Kg (Groups III and IV) once a week for two weeks. Fifteen weeks later, the animals were euthanized. RESULTS: FED promoted weight gain in Groups II and IV compared to Groups I and III, respectively. The groups did not differ with regard to the total number of ACF. The Chi-square test revealed no predominance of the presence of foci with <4 crypts. However, foci with ≥5 crypts were proportionally more prevalent in Group III than in Group IV (p=0.043). CONCLUSION: The administration of polyunsaturated fatty acids did not interfere with the formation of aberrant crypt foci, but reduced ACF multiplicity, exercising an attenuating effect on carcinogenesis.

OBJETIVO: Determinar se uma dieta hipercalórica, hiperlipídica, rica em ácidos graxos poliinsaturados (FED) tem influência na formação de focos de cripta aberrante (FCA) em mucosa cólica de ratos Wistar expostos ao azoximetano (AOM). MÉTODOS: Com oito semanas de vida, os ratos foram distribuídos em quatro grupos: Grupo I: Dieta padrão (SD) sem AOM; Grupo II: FED, sem AOM; Grupo III: SD, com AOM; Grupo IV: FED com AOM. Com 16 semanas, os animais dos grupos I e II receberam injeções intraperitoneais de solução salina 0,9 por cento, enquanto os dos grupos III e IV receberam AOM na dose de 15mg/Kg de peso, 1 vez por semana por duas semanas. Quinze semanas após, os animais foram mortos. RESULTADOS: FED promoveu aumento de peso nos grupos II e IV em relação aos grupos I e III. Não houve aumento significante no número total de FCA entre os grupos. Em relação à multiplicidade das criptas por FCA, o teste do qui-quadrado mostrou que não houve predominância da presença <4 criptas por foco. Contudo, focos ≥5 criptas foram proporcionalmente mais prevalentes no grupo III que no grupo IV (p=0,043). CONCLUSÃO: Os ácidos graxos poliinsaturados não interferem na formação de focos de cripta aberrante, contudo reduz sua multiplicidade, exercendo efeito atenuador na carcinogênese.

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PURPOSE: To study the antitumor action of Tabebuia avellanedae in experimentally induced colon carcinogenesis by azoxymethane in mice. METHODS: Fifty (n=50) mice were divided into five groups: in group I azoxymethane (AOM) was administered, in Group II - β-lapachone, in group III - vehicle (diluent) and in group IV - vehicle + AOM and finally in group V - β-lapachone + AOM. RESULTS: It was observed the presence of aberrant crypt foci in all animals of groups I and IV, 50 percent in group II and 90 percent in group V. CONCLUSION: The β-lapachone extracted from the Tabebuia avellanedae showed no protective effect of lesions induced by azoxymethane in colon of mice.(AU)

OBJETIVO: Estudar a ação antitumoral da Tabebuia avellanedae (Ipê-Roxo) na carcinogênese colônica induzida experimentalmente pelo azoximetano em camundongos. MÉTODOS: Foram utilizados 50 camundongos divididos em 5 grupos: grupo I administrado Azoximetano (AOM); grupo II - β-lapachona; grupo III - veículo (diluente); grupo IV - veículo + AOM; e grupo V - β-lapachona + AOM. RESULTADOS: Observou-se presença de focos de criptas aberrantes em todos os animais dos grupos I e IV, 50 por cento no grupo II e 90 por cento no grupo V. CONCLUSÃO: A β-lapachona extraída da Tabebuia avellanedae não apresentou efeito protetor das lesões induzidas pelo azoximetano em cólon de camundongos.(AU)

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PURPOSE: To study the antitumor action of Tabebuia avellanedae in experimentally induced colon carcinogenesis by azoxymethane in mice. METHODS: Fifty (n=50) mice were divided into five groups: in group I azoxymethane (AOM) was administered, in Group II - β-lapachone, in group III - vehicle (diluent) and in group IV - vehicle + AOM and finally in group V - β-lapachone + AOM. RESULTS: It was observed the presence of aberrant crypt foci in all animals of groups I and IV, 50 percent in group II and 90 percent in group V. CONCLUSION: The β-lapachone extracted from the Tabebuia avellanedae showed no protective effect of lesions induced by azoxymethane in colon of mice.

OBJETIVO: Estudar a ação antitumoral da Tabebuia avellanedae (Ipê-Roxo) na carcinogênese colônica induzida experimentalmente pelo azoximetano em camundongos. MÉTODOS: Foram utilizados 50 camundongos divididos em 5 grupos: grupo I administrado Azoximetano (AOM); grupo II - β-lapachona; grupo III - veículo (diluente); grupo IV - veículo + AOM; e grupo V - β-lapachona + AOM. RESULTADOS: Observou-se presença de focos de criptas aberrantes em todos os animais dos grupos I e IV, 50 por cento no grupo II e 90 por cento no grupo V. CONCLUSÃO: A β-lapachona extraída da Tabebuia avellanedae não apresentou efeito protetor das lesões induzidas pelo azoximetano em cólon de camundongos.

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PURPOSE: To study the protein Fas ligand (FasL) on the expression of apoptosis, using a model of oxidative stress induced by azoxymethane (AOM), in the crypt of colon in rats. METHODS: Wistar rats (n=14) were assigned into two groups: control (n=7) and AOM (n=7). A single subcutaneous administration of AOM (5mg/kg) or saline solution was performed at the beginning of third week and after three hours samples of proximal colon were collected. The expression of FasL was quantified (Software ImageLab) in percentage of areas in the top, base and all crypt. Results were expressed as mean ± sd (Shapiro-Wilks test and t Student test) (p < 0.05). RESULTS: In the animals of CG there was no significant difference between the FasL expression of the top (10.75±3.33) and basal (11.14±3.53) colon crypt (p=0.34293740). In the animals of AOM there was no significant difference between the FasL expression of the top (8.86±4.19) and basal (8.99±4.08) colon crypt (p=0.78486003). In the animals of CG (10.95±3.43) and AOM (8.92±4.13) there was a significant difference of the FasL expression (p=0.026466821). A significantly decrease on the FasL expression was observed in the animals of CG (10.75±3.33) and AOM (8.86±4.19) in the top crypt (p=0.00003755*). A significant decrease was also observed in the animals of CG (11.14±3.53) and AOM (8.99±4.08) in the basal colon crypt (p=0.00000381**). CONCLUSION: Azoxymethane induce the oxidative stress and the significantly decrease of FasL expression, although there is no significant difference between basal and top of colon crypt linked to consumption-activation of Fas ligand.(AU)

OBJETIVO: Avaliar o marcador de apoptose Fas ligante (FasL) em um modelo de estresse oxidativo induzido pelo azoximetano (AOM) na cripta de cólon em ratos. MÉTODOS: 14 ratos Wistar foram distribuídos em dois grupos: controle (n=7) e AOM (n=7). A AOM (5mg/kg) ou solução salina foi aplicada via subcutânea e a coleta de amostras de colo proximal ocorreu 3 horas após. A FasL foi quantificada pelo percentual de áreas no topo, base e toda a cripta. Os resultados foram submetidos aos testes de Shapiro-Wilks e t de Student (p < 0,05). RESULTADOS: No grupo GC, não houve diferença significativa entre a expressão da FasL no topo (10,75 ± 3,33) e base (11,14 ± 3,53) da cripta (p=0,34293740). No grupo AOM não houve diferença significativa entre a expressão da FasL no topo (8,86 ± 4,19) e base (8,99 ± 4,08) e cripta (p=0,78486003). No grupo GC (10,95 ± 3,43) e AOM (8,92 ± 4,13), houve uma diferença significativa da expressão da FasL (p=0,026466821). Redução significativa na expressão da FasL ocorreu nos em GC (10,75 ± 3,33) e AOM (8,86 ± 4,19) no topo da cripta (p = 0,00003755*). Foi observada diminuição significativa em GC (11,14 ± 3,53) e AOM (8,99 ± 4,08) na base da cripta (p=0,00000381**). CONCLUSÃO: Azoximetano induziu o estresse oxidativo identificado pela diminuição significativa da expressão da FasL, embora não haja diferença significativa entre a base e parte superior da cripta associada à ativação de consumo do FasL.(AU)

Assuntos

RESUMO

PURPOSE: To study the protein Fas ligand (FasL) on the expression of apoptosis, using a model of oxidative stress induced by azoxymethane (AOM), in the crypt of colon in rats. METHODS: Wistar rats (n=14) were assigned into two groups: control (n=7) and AOM (n=7). A single subcutaneous administration of AOM (5mg/kg) or saline solution was performed at the beginning of third week and after three hours samples of proximal colon were collected. The expression of FasL was quantified (Software ImageLab) in percentage of areas in the top, base and all crypt. Results were expressed as mean ± sd (Shapiro-Wilks test and t Student test) (p < 0.05). RESULTS: In the animals of CG there was no significant difference between the FasL expression of the top (10.75±3.33) and basal (11.14±3.53) colon crypt (p=0.34293740). In the animals of AOM there was no significant difference between the FasL expression of the top (8.86±4.19) and basal (8.99±4.08) colon crypt (p=0.78486003). In the animals of CG (10.95±3.43) and AOM (8.92±4.13) there was a significant difference of the FasL expression (p=0.026466821). A significantly decrease on the FasL expression was observed in the animals of CG (10.75±3.33) and AOM (8.86±4.19) in the top crypt (p=0.00003755*). A significant decrease was also observed in the animals of CG (11.14±3.53) and AOM (8.99±4.08) in the basal colon crypt (p=0.00000381**). CONCLUSION: Azoxymethane induce the oxidative stress and the significantly decrease of FasL expression, although there is no significant difference between basal and top of colon crypt linked to consumption-activation of Fas ligand.

OBJETIVO: Avaliar o marcador de apoptose Fas ligante (FasL) em um modelo de estresse oxidativo induzido pelo azoximetano (AOM) na cripta de cólon em ratos. MÉTODOS: 14 ratos Wistar foram distribuídos em dois grupos: controle (n=7) e AOM (n=7). A AOM (5mg/kg) ou solução salina foi aplicada via subcutânea e a coleta de amostras de colo proximal ocorreu 3 horas após. A FasL foi quantificada pelo percentual de áreas no topo, base e toda a cripta. Os resultados foram submetidos aos testes de Shapiro-Wilks e t de Student (p < 0,05). RESULTADOS: No grupo GC, não houve diferença significativa entre a expressão da FasL no topo (10,75 ± 3,33) e base (11,14 ± 3,53) da cripta (p=0,34293740). No grupo AOM não houve diferença significativa entre a expressão da FasL no topo (8,86 ± 4,19) e base (8,99 ± 4,08) e cripta (p=0,78486003). No grupo GC (10,95 ± 3,43) e AOM (8,92 ± 4,13), houve uma diferença significativa da expressão da FasL (p=0,026466821). Redução significativa na expressão da FasL ocorreu nos em GC (10,75 ± 3,33) e AOM (8,86 ± 4,19) no topo da cripta (p = 0,00003755*). Foi observada diminuição significativa em GC (11,14 ± 3,53) e AOM (8,99 ± 4,08) na base da cripta (p=0,00000381**). CONCLUSÃO: Azoximetano induziu o estresse oxidativo identificado pela diminuição significativa da expressão da FasL, embora não haja diferença significativa entre a base e parte superior da cripta associada à ativação de consumo do FasL.

Assuntos