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Bol. latinoam. Caribe plantas med. aromát ; 21(1): 66-80, ene. 2022. ilus, tab
Article in English | LILACS | ID: biblio-1372378


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.

Animals , Rats , Plant Extracts/administration & dosage , Anticarcinogenic Agents/administration & dosage , Colonic Neoplasms/drug therapy , Melastomataceae/chemistry , Organ Size/drug effects , Body Weight/drug effects , Chromatography, High Pressure Liquid , Rats, Sprague-Dawley , Colon/pathology , Plant Leaves , Methanol , Phenolic Compounds , Aberrant Crypt Foci , Carcinogenesis/drug effects , Antioxidants
Rev. cuba. endocrinol ; 27(3): 69-79, sep.-dic. 2016. ilus, tab
Article in Spanish | LILACS | ID: biblio-830470


Antecedentes: la metformina, fármaco económico y seguro, ha demostrado mejorar el pronóstico de varios tipos de cánceres. Objetivo: revisar los aspectos más relevantes de la relación entre la diabetes mellitus, la metformina y el cáncer. Desarrollo: la diabetes mellitus, en especial la tipo 2, se relaciona con algunos cánceres (mama, hígado, páncreas, ginecológico, vejiga, colon y recto), y en el sexo masculino, aumenta su recurrencia y la mortalidad. Los mecanismos responsables de esta relación no están del todo esclarecidos. La insulina y el factor de crecimiento similar a la insulina en un estado de hiperinsulinismo e insulinorresistencia, pudieran desempeñar un papel fundamental en el desarrollo de cáncer, así como otros factores de riesgo comunes a la diabetes mellitus y al cáncer (alimentación no saludable, sedentarismo, adicciones, edad, sexo, etnia y raza). La proteína liver kinase B1 se ha identificado como una proteína supresora tumoral, y al unirse con la metformina interrumpe el complejo 1 de la cadena respiratoria mitocondrial, y conduce a la disminución de la síntesis de trifosfato de adenosin, y al aumento del cociente proteína activada por mitógenos-trifosfato de adenosin en el espacio intracelular. Los quimioterápicos, esteroides y antiandrógenos, pueden afectar negativamente el metabolismo hidrocarbonado. Algunas drogas antihiperglucemiantes se han relacionado a cánceres específicos, aunque las evidencias son pobres, indirectas y controversiales. Conclusiones: la metformina pudiera utilizarse en la prevención y el tratamiento de algunos cánceres, y reducir su recurrencia y la mortalidad. Parece existir una relación entre cáncer y la diabetes mellitus, aunque muchos aspectos quedan por dilucidar, como el papel desempeñado por los fármacos anticancerígenos y antihiperglucemiantes utilizados en ambas entidades(AU)

Background: metformin, a safe inexpensive drug, has proved to improve the prognosis of several types of cancer. Objective: to review the most relevant aspects of the relationship among diabetes mellitus, metformin and cancer. Development: diabetes mellitus, particularly type 2, is related to some kinds of cancer (breast, liver, pancreas, gynecological, gallbladder, colon and rectum), and its recurrence and mortality increase in men. The mechanism behind this relationship is not fully clarified. Insulin and insulin-like growth factor under hyperinsulinism and insulin resistance conditions may play a fundamental role in developing cancer as well as other common risk factors for diabetes mellitus and cancer (unhealthy feeding, sedentary lifestyle, addictions, age, sex, ethnic group and race). Liver kinase B1 protein has been identified as tumor suppressor protein which binds the metformin to impair the mitochondrial respiratory chain complex I and leads to reduction of adenosine triphosphate synthesis and to the increase of mytogen-activated protein-adenosine triphosphate quotient in the intracellular space. Chemotherapeutic, steroid and anti-androgen drugs may negatively affect the hydrocarbon metabolism. Some antihyperglycemic drugs have been related to specific cancers, although the evidence is still poor, indirect and controversial. Conclusions: metformin may be used to prevent and treat some types of cancer and to reduce recurrence and mortality. There seems to be some relationship between cancer and diabetes mellitus, even when many aspects remain to be ascertained such as the role played by anticancer and antihyperglycemic drugs intended to treat both diseases(AU)

Humans , Male , Diabetes Mellitus/drug therapy , Metformin/therapeutic use , Neoplasms/drug therapy , Receptors, Growth Factor/drug effects , Anticarcinogenic Agents/administration & dosage , Metformin/adverse effects , Neoplasms/prevention & control , Risk Factors
Braz. j. med. biol. res ; 45(9): 841-850, Sept. 2012. ilus
Article in English | LILACS | ID: lil-646329


The combined treatment with histone deacetylase inhibitors (HDACi) and retinoids has been suggested as a potential epigenetic strategy for the control of cancer. In the present study, we investigated the effects of treatment with butyrate, a dietary HDACi, combined with vitamin A on MCF-7 human breast cancer cells. Cell proliferation was evaluated by the crystal violet staining method. MCF-7 cells were plated at 5 x 10(4) cells/mL and treated with butyrate (1 mM) alone or combined with vitamin A (10 µM) for 24 to 120 h. Cell proliferation inhibition was 34, 10 and 46% following treatment with butyrate, vitamin A and their combination, respectively, suggesting that vitamin A potentiated the inhibitory activities of butyrate. Furthermore, exposure to this short-chain fatty acid increased the level of histone H3K9 acetylation by 9.5-fold (Western blot), but not of H4K16, and increased the expression levels of p21WAF1 by 2.7-fold (Western blot) and of RARβ by 2.0-fold (quantitative real-time PCR). Our data show that RARβ may represent a molecular target for butyrate in breast cancer cells. Due to its effectiveness as a dietary HDACi, butyrate should be considered for use in combinatorial strategies with more active retinoids, especially in breast cancers in which RARβ is epigenetically altered.

Female , Humans , Anticarcinogenic Agents/pharmacology , Breast Neoplasms/pathology , Butyrates/pharmacology , Cell Proliferation/drug effects , DNA Methylation/drug effects , Histone Deacetylase Inhibitors/pharmacology , Vitamin A/pharmacology , Anticarcinogenic Agents/administration & dosage , Butyrates/administration & dosage , Histone Deacetylase Inhibitors/administration & dosage , Vitamin A/administration & dosage
Braz. j. med. biol. res ; 39(8): 1115-1119, Aug. 2006. tab
Article in English | LILACS | ID: lil-433171


The consumption of tomatoes and tomato products has been associated with a reduced risk of prostate cancer. We observed a decrease of 10.77 percent in prostate-specific antigen (PSA) levels in patients with benign prostate hyperplasia who were submitted to daily ingestion of tomato paste. This was an experimental rather than a controlled study with a sample of 43 men ranging in age from 45 to 75 years, all with histological diagnoses of benign prostate hyperplasia and plasma PSA levels of 4-10 ng/mL. All patients received 50 g of tomato paste once a day for 10 consecutive weeks and PSA levels were analyzed before, during and after the consumption of tomato paste. ANOVA for repeated measures was used to compare PSA levels before, during and after the consumption of tomato paste. The mean ± SD PSA level was 6.51 ± 1.48 ng/mL at baseline and 5.81 ± 1.58 ng/mL (P = 0.005) after 10 weeks. Acceptance was good in 88.3, regular in 9.3, and poor in 2.3 percent of the patients. Dietary ingestion of 50 g of tomato paste per day for 10 weeks significantly reduced mean plasma PSA levels in patients with benign prostate hyperplasia, probably as a result of the high amount of lycopene in tomato paste. This was not a prostate cancer prevention study, but showed some action of tomato paste in prostate biology. The development of prostate cancer is typically accompanied by an increase in plasma PSA levels, thus any intervention that affects plasma PSA levels can suggest an impact in the progression of disease.

Aged , Humans , Male , Middle Aged , Anticarcinogenic Agents/administration & dosage , Carotenoids/administration & dosage , Solanum lycopersicum/chemistry , Prostate-Specific Antigen/blood , Prostatic Hyperplasia/diet therapy , Analysis of Variance , Nutritive Value , Prostate-Specific Antigen/drug effects , Prostatic Hyperplasia/blood
Indian J Cancer ; 2005 Jan-Mar; 42(1): 15-24
Article in English | IMSEAR | ID: sea-50137


Dietary behavior seems to be an important modifiable determinant for the risk of cancer. The evidences from several epidemiological studies suggest that higher intakes of fruits and vegetables have been associated with lower risk of cancer. Dietary phenolic and polyphenolic substances, terpenoids, dietary fibers, fish oils, some micronutrients present in foods of both plant and animal origin, and a reduction of caloric intake appear to inhibit the process of cancer development. Many dietary factors possess antioxidant and anti-inflammatory properties and cause induction of phase II enzymes like glutathione-S-transferases. It has been suggested that cruciferous vegetables play an important role in cancer prevention, and their chemopreventive effects are due to high glucosinolate content which under enzymatic hydrolysis produces bioactive compound isothiocyanates. Further, isothiocyanates of a wide variety of cruciferous vegetables are powerful inhibitors of carcinogenesis in experimental animal models. Several flavonoids present in fruits, tea, soya beans, etc. may be useful as cancer preventive agents. Similarly, ellagic acid, perillyl alcohol and resveratrol found in various fruits may have chemoprotective effect. Moreover, different vanilloids such as curcumin and gingerol have been shown to possess antioxidative properties. Nevertheless, in spite of several studies, still the effects of various ingredients are not clearly distinguished. In human, little convincing evidence has been established for the proposed protective effects of dietary constituents. It is an important future research goal to provide necessary evidences to support the chemopreventive role of different dietary factors, and also to clarify misunderstandings in this perplexing area.

Anticarcinogenic Agents/administration & dosage , Diet , Humans , Neoplasms/prevention & control
Article in English | IMSEAR | ID: sea-37837


The modifying effects of dietary administration of protocatechuic acid (PCA) during the progression phase of tongue carcinogenesis initiated with 4-nitroquinoline 1-oxide (4-NQO) were investigated in male F344 rats. For tumor progression we developed a new animal model, where rats initiated by 4-week treatment of 20 ppm 4-NQO in drinking water, received four cycles of 20 ppm 4-NQO to induce advanced tongue cancer (one cycle: 2 weeks of 4-NQO followed by 2 weeks of tap water), starting at 14 weeks after the initiation. In this model, metastasis of tongue cancer occurred in lungs. Starting two weeks before the cycle treatment with 4-NQO, animals were fed the 2000 ppm PCA containing diet and continued on this diet until the end of the study. At the termination of the experiment (week 32), the incidences of tongue neoplasms and preneoplastic lesions, polyamine levels in the tongue tissue, and cell proliferation activity estimated by morphometric analysis of silver-stained nucleolar organizer regions protein were compared among the groups. Feeding with PCA containing diet during the progression phase significantly decreased the occurrence of advanced tongue squamous cell carcinoma with metastasis (P<0.05) and preneoplasia (hyperplasia and dysplasia) (P<0.001). In addition, PCA exposure decreased polyamine levels in the tongue tissue (P<0.001) during progression phase. Our results suggest that dietary PCA inhibits progression of 4-NQO-induced oral carcinogenesis, and such inhibition might be related to suppression of cell proliferation by PCA.

4-Nitroquinoline-1-oxide , Animals , Anticarcinogenic Agents/administration & dosage , Biomarkers/analysis , Carcinoma, Squamous Cell/pathology , Diet , Hydroxybenzoates/administration & dosage , Male , Polyamines/analysis , Quinolones , Rats , Rats, Inbred F344 , Tongue Neoplasms/chemically induced