scholarly journals INHIBITION OF CARSINOGENESIS BY SEED AND SOYBEAN MEAL EXTRACT IN COLON OF MICE: APOPTOSIS AND DYSPLASIA

2017 ◽  
Vol 10 (4) ◽  
pp. 123
Author(s):  
Ade Arsianti Arsianti ◽  
Anindini Winda Amalia ◽  
Kusmardi Suid ◽  
Berna Elya
Keyword(s):  
Colon Cancer ◽  
Soybean Meal ◽  
Sodium Sulfate ◽  
Xenograft Model ◽  
Public Health Problem ◽  
Experimental Models ◽  
Aberrant Crypt Foci ◽  
Dextran Sodium Sulfate ◽  
Major Public Health Problem ◽  
Preneoplastic Lesions

Objective: Colon cancer is a major public health problem. Soybean has demonstrated chemopreventive and anti-cancer. Here, we have investigated the effect of a standardized seed and soybean meal extract with content of  lunasin, here named  GE and SE. They are botanical drug substance in experimental models of colon cancer in vivo.Methods:The effect of  GE and SEwere examined onthe preneoplastic lesions (aberrant crypt foci), polyps and tumours induced by the carcinogenic agentazoxymethane (AOM) (10 mg/kg) and dextran sodium sulfate (DSS) 2%  as well as in a xenograft model of colon cancer in mice.Results:.GE and SE increased apoptosis (p = 0,001). GE (150 mg/kg) has the highest impact level of apoptosis (p = 0,009). GE and  SE decreased dysplasia (p = 0,024). GE (200 mg/kg) has the highest impact level of dysplasia (p = 0,002) and SE (200 mg/kg) has the second impact level of dysplasia (p = 0,003).Conclusions: GE and SE inhibition of colon carsinogenesis with incrase level of apoptosis and decrease level of dysplasiaKeyword: soybean, lunasin, colon cancer, azoxymethane, dextran sodium sulfate, apoptosis, dysplasia

scholarly journals Animal Models of Undernutrition and Enteropathy as Tools for Assessment of Nutritional Intervention.

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2233 ◽  
Author(s):  
Salameh ◽  
Morel ◽  
Zeilani ◽  
Déchelotte ◽  
Marion-Letellier
Keyword(s):  
Growth Failure ◽  
Public Health Problem ◽  
Nutritional Intervention ◽  
Experimental Models ◽  
Major Public Health Problem ◽  
Gut Function ◽  
Environmental Enteric Dysfunction ◽  
Clinical Models ◽  
Novel Therapeutic Strategies ◽  
The Impact

: Undernutrition is a major public health problem leading to 1 in 5 of all deaths in children under 5 years. Undernutrition leads to growth stunting and/or wasting and is often associated with environmental enteric dysfunction (EED). EED mechanisms leading to growth failure include intestinal hyperpermeability, villus blunting, malabsorption and gut inflammation. As non-invasive methods for investigating gut function in undernourished children are limited, pre-clinical models are relevant to elucidating the pathophysiological processes involved in undernutrition and EED, and to identifying novel therapeutic strategies. In many published models, undernutrition was induced using protein or micronutrient deficient diets, but these experimental models were not associated with EED. Enteropathy models mainly used gastrointestinal injury triggers. These models are presented in this review. We found only a few studies investigating the combination of undernutrition and enteropathy. This highlights the need for further developments to establish an experimental model reproducing the impact of undernutrition and enteropathy on growth, intestinal hyperpermeability and inflammation, that could be suitable for preclinical evaluation of innovative therapeutic intervention.

scholarly journals ANIMAL MODELS FOR THE STUDY OF LEISHMANIASIS IMMUNOLOGY

2014 ◽  
Vol 56 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Elsy Nalleli Loria-Cervera ◽  
Fernando Jose Andrade-Narvaez
Keyword(s):  
Animal Models ◽  
Human Disease ◽  
Public Health Problem ◽  
Leishmania Species ◽  
Experimental Models ◽  
Sand Fly ◽  
Leishmania Infection ◽  
Major Public Health Problem ◽  
Wild Rodents ◽  
Experimental Conditions

Leishmaniasis remains a major public health problem worldwide and is classified as Category I by the TDR/WHO, mainly due to the absence of control. Many experimental models like rodents, dogs and monkeys have been developed, each with specific features, in order to characterize the immune response to Leishmania species, but none reproduces the pathology observed in human disease. Conflicting data may arise in part because different parasite strains or species are being examined, different tissue targets (mice footpad, ear, or base of tail) are being infected, and different numbers (“low” 1×102 and “high” 1×106) of metacyclic promastigotes have been inoculated. Recently, new approaches have been proposed to provide more meaningful data regarding the host response and pathogenesis that parallels human disease. The use of sand fly saliva and low numbers of parasites in experimental infections has led to mimic natural transmission and find new molecules and immune mechanisms which should be considered when designing vaccines and control strategies. Moreover, the use of wild rodents as experimental models has been proposed as a good alternative for studying the host-pathogen relationships and for testing candidate vaccines. To date, using natural reservoirs to study Leishmania infection has been challenging because immunologic reagents for use in wild rodents are lacking. This review discusses the principal immunological findings against Leishmania infection in different animal models highlighting the importance of using experimental conditions similar to natural transmission and reservoir species as experimental models to study the immunopathology of the disease.

scholarly journals Pathogenesis of Cerebral Malaria: Recent Experimental Data and Possible Applications for Humans

2001 ◽  
Vol 14 (4) ◽  
pp. 810-820 ◽  
Author(s):  
Jinning Lou ◽  
Ralf Lucas ◽  
Georges E. Grau
Keyword(s):  
Endothelial Cells ◽  
Cerebral Malaria ◽  
Public Health Problem ◽  
Major Complication ◽  
Experimental Models ◽  
Soluble Form ◽  
Recent Experimental Data ◽  
Major Public Health Problem

SUMMARY Malaria still is a major public health problem, partly because the pathogenesis of its major complication, cerebral malaria, remains incompletely understood. Experimental models represent useful tools to better understand the mechanisms of this syndrome. Here, data generated by several models are reviewed both in vivo and in vitro; we propose that some pathogenic mechanisms, drawn from data obtained from experiments in a mouse model, may be instrumental in humans. In particular, tumor necrosis factor (TNF) receptor 2 is involved in this syndrome, implying that the transmembrane form of TNF may be more important than the soluble form of the cytokine. It has also been shown that in addition to differences in immune responsiveness between genetically resistant and susceptible mice, there are marked differences at the level of the target cell of the lesion, namely, the brain endothelial cell. In murine cerebral malaria, a paradoxical role of platelets has been proposed. Indeed, platelets appear to be pathogenic rather than protective in inflammatory conditions because they can potentiate the deleterious effects of TNF. More recently, it has been shown that interactions among platelets, leukocytes, and endothelial cells have phenotypic and functional consequences for the endothelial cells. A better understanding of these complex interactions leading to vascular injury will help improve the outcome of cerebral malaria.

scholarly journals mTOR Kinase: A Possible Pharmacological Target in the Management of Chronic Pain

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Lucia Lisi ◽  
Paola Aceto ◽  
Pierluigi Navarra ◽  
Cinzia Dello Russo
Keyword(s):  
Chronic Pain ◽  
Neuropathic Pain ◽  
Mammalian Target Of Rapamycin ◽  
Public Health Problem ◽  
Experimental Models ◽  
Major Public Health Problem ◽  
Major Mechanism ◽  
Mtor Kinase ◽  
Pain Transmission ◽  
Pharmacological Target

Chronic pain represents a major public health problem worldwide. Current pharmacological treatments for chronic pain syndromes, including neuropathic pain, are only partially effective, with significant pain relief achieved in 40–60% of patients. Recent studies suggest that the mammalian target of rapamycin (mTOR) kinase and downstream effectors may be implicated in the development of chronic inflammatory, neuropathic, and cancer pain. The expression and activity of mTOR have been detected in peripheral and central regions involved in pain transmission. mTOR immunoreactivity was found in primary sensory axons, in dorsal root ganglia (DRG), and in dorsal horn neurons. This kinase is a master regulator of protein synthesis, and it is critically involved in the regulation of several neuronal functions, including the synaptic plasticity that is a major mechanism leading to the development of chronic pain. Enhanced activation of this pathway is present in different experimental models of chronic pain. Consistently, pharmacological inhibition of the kinase activity turned out to have significant antinociceptive effects in several experimental models of inflammatory and neuropathic pain. We will review the main evidence from animal and human studies supporting the hypothesis that mTOR may be a novel pharmacological target for the management of chronic pain.

Chemopreventive effects of aloin against 1,2-dimethylhydrazine-induced preneoplastic lesions in the colon of Wistar rats

2013 ◽  
Vol 33 (2) ◽  
pp. 148-163 ◽  
Author(s):  
OO Hamiza ◽  
MU Rehman ◽  
R Khan ◽  
M Tahir ◽  
AQ Khan ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Wistar Rats ◽  
Aberrant Crypt Foci ◽  
Nuclear Antigen ◽  
Protective Mechanism ◽  
Antioxidant Enzyme Activities ◽  
Protective Agent ◽  
Preneoplastic Lesions ◽  
Markers Of Inflammation ◽  
Factor Α

Chemoprevention opens new window in the prevention of all types of cancers including colon cancer. Aloin, an anthracycline in plant pigment, can be utilized as a protective agent in cancer induction. In the present study, we have evaluated the chemopreventive efficacy of aloin against 1,2-dimethylhydrazine (DMH)-induced preneoplastic lesions in the colon of Wistar rats. DMH-induced aberrant crypt foci (ACF) and mucin-depleted foci (MDF) have been used as biomarkers of colon cancer. Efficacy of aloin against the colon toxicity was evaluated in terms of biochemical estimation of antioxidant enzyme activities, lipid peroxidation, ACF, MDF, histopathological changes, and expression levels of molecular markers of inflammation and tumor promotion. Aloin pretreatment ameliorates the damaging effects induced by DMH through a protective mechanism that involved reduction in increased oxidative stress enzymes ( p < 0.001), ACF, MDF, cyclooxygenase-2, inducible nitric oxide synthase, interleukin-6, proliferating cell nuclear antigen protein expression, and tumor necrosis factor-α ( p < 0.001) release. From the results, it could be concluded that aloin clearly protects against chemically induced colon toxicity and acts reasonably by inducing antioxidant level, anti-inflammatory and antiproliferative markers.

scholarly journals Antitumor Activity of Monoterpenes Found in Essential Oils

2014 ◽  
Vol 2014 ◽  
pp. 1-35 ◽  
Author(s):  
Marianna Vieira Sobral ◽  
Aline Lira Xavier ◽  
Tamires Cardoso Lima ◽  
Damião Pergentino de Sousa
Keyword(s):  
Public Health ◽  
Antitumor Activity ◽  
Essential Oils ◽  
Genetic Disease ◽  
Public Health Problem ◽  
Mechanisms Of Action ◽  
Experimental Models ◽  
Major Public Health Problem ◽  
Bioactive Substances ◽  
Chemical Structures

Cancer is a complex genetic disease that is a major public health problem worldwide, accounting for about 7 million deaths each year. Many anticancer drugs currently used clinically have been isolated from plant species or are based on such substances. Accumulating data has revealed anticancer activity in plant-derived monoterpenes. In this review the antitumor activity of 37 monoterpenes found in essential oils is discussed. Chemical structures, experimental models, and mechanisms of action for bioactive substances are presented.

Intermittent hypoxia promotes carcinogenesis in azoxymethane and dextran sodium sulfate‐induced colon cancer model

2019 ◽  
Vol 58 (5) ◽  
pp. 654-665 ◽  
Author(s):  
Dae Wui Yoon ◽  
Yi‐Sook Kim ◽  
Soyoung Hwang ◽  
Roza Khalmuratova ◽  
Mingyu Lee ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Sodium Sulfate ◽  
Intermittent Hypoxia ◽  
Dextran Sodium Sulfate ◽  
Cancer Model

scholarly journals Effects of Total Western Diet and Wheat Class and Fraction on Preneoplastic Colon Cancer Risk

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 262-262
Author(s):  
Allison Bailey ◽  
Daniel Gallaher ◽  
Senay Simsek
Keyword(s):  
Colon Cancer ◽  
Wnt Signaling Pathway ◽  
Nutritional Composition ◽  
Western Diet ◽  
Aberrant Crypt Foci ◽  
Stem Cell Marker ◽  
Beta Catenin ◽  
Preneoplastic Lesions ◽  
White Wheat ◽  
Background Diet

Abstract Objectives Colon cancer (CC) is a leading cause of cancer-related deaths worldwide and is particularly prevalent among persons consuming a Western-style diet. Red wheat, compared to white wheat, may reduce CC risk, as measured by reductions in colonic preneoplastic lesions (aberrant crypt foci; ACF). Rodent studies typically use a purified diet (AIN-93G) as the background diet, but due to its optimal nutritional composition, it may mask some effects of chemopreventive bioactives. The Total Western Diet (TWD), matched to the 50th percentile of US diets using NHANES data, has greater translational integrity to humans. This study aims to elucidate effects of background diet (AIN-93G vs TWD), wheat class (red vs white), and wheat fraction (whole vs refined vs testa layer) when fed during the post-initiation period. Methods Male Wistar rats (n = 83) were injected with the colon-specific carcinogen 1,2-dimethylhydrazine (twice, one week apart) to induce ACF. Five days after final injection, diets containing either AIN-93G or TWD background and various fractions of red and white wheat were fed for 10 weeks. Results No statistically significant differences in ACF number were found due to background diet. However, a statistically significant decrease in ACF was found in rats fed the TWD + whole red wheat (RW) relative to the TWD and the AIN-93G + refined red wheat diets. The short-chain fatty acid (SCFA) butyrate may act as a histone deacetylase to prevent CC. TWD + RW significantly increased total SCFAs as well as total butyrate compared to all other groups. TWD had significantly decreased total SCFAs and total butyrate compared to AIN-93G. Preliminary immunohistochemical results show that neither beta-catenin (part of the Wnt signaling pathway frequently dysregulated in CC) nor doublecortin-like kinase 1 (DCLK1; a putative cancer stem cell marker) staining of ACF significantly differ between TWD and TWD + RW. Conclusions The butyrate amount in cecal contents did not correlate with the staining intensity within ACF for beta-catenin or DCLK1 biomarkers, which does not support a role for high total butyrate reducing the risk of CC. Red wheat, when fed as part of the TWD, may reduce CC risk. Funding Sources Healthy Foods, Healthy Lives Institute, University of Minnesota.

scholarly journals Soy Saponins Meditate the Progression of Colon Cancer in Rats by Inhibiting the Activity of β-Glucuronidase and the Number of Aberrant Crypt Foci but Not Cyclooxygenase-2 Activity

ISRN Oncology ◽  
2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Yu-Wei Guo ◽  
Yue-Hwa Chen ◽  
Wan-Chun Chiu ◽  
Hsiang Liao ◽  
Shyh-Hsiang Lin
Keyword(s):  
Colon Cancer ◽  
Protein Expression ◽  
Research Methods ◽  
Colonic Mucosa ◽  
Cyclooxygenase 2 ◽  
Aberrant Crypt Foci ◽  
Preneoplastic Lesions ◽  
Pge2 Level ◽  
Cox 2 ◽  
Different Doses

Objective. The effect of extracted crude soybean saponins on preneoplastic lesions, aberrant crypt foci (ACF), and the related mechanism were investigated. Research Methods and Procedures. Rats were assigned into five groups according to different doses of extracted crude soybean saponins and received 1,2-dimethylhydrazine (DMH) injection in week 5. In week 15, all rats were sacrificed. The number of ACFs, the cyclooxygenase-2 (COX-2) protein expression, the level of prostaglandins E2 (PGE2), and the activity of β-glucuronidase were examined. Results. Results revealed that the consumption of extracted crude soybean saponins decreased the number of ACFs and the activity of β-glucuronidase in rats, while the expression of COX-2 protein and PGE2 level were not affected. Conclusions. Soybean saponins were effective in inhibiting colon cancer by downregulating the activity of β-glucuronidase in colonic mucosa but not the COX-2 protein expression and PGE2 level.

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