ubiquinone has been researched along with Colonic-Neoplasms* in 7 studies
1 trial(s) available for ubiquinone and Colonic-Neoplasms
6 other study(ies) available for ubiquinone and Colonic-Neoplasms
Article | Year |
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Antroquinonol, a Ubiquinone Derivative from the Mushroom Antrodia camphorata, Inhibits Colon Cancer Stem Cell-like Properties: Insights into the Molecular Mechanism and Inhibitory Targets.
Topics: Antrodia; beta Catenin; Cell Line, Tumor; Cell Proliferation; Colonic Neoplasms; Humans; Molecular Docking Simulation; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Signal Transduction; Ubiquinone | 2017 |
Ubiquinol reduces muscle wasting but not fatigue in tumor-bearing mice.
Fatigue is the most common and distressing symptom reported by cancer patients during and after treatment. Tumor growth increases oxidative stress and cytokine production, which causes skeletal muscle wasting and cardiac dysfunction. The purpose of this study was to determine whether treatment with the antioxidant ubiquinol improves muscle mass, cardiac function, and behavioral measures of fatigue in tumor-bearing mice.. Adult female mice were inoculated with colon26 tumor cells. Half the control and tumor-bearing mice were administered ubiquinol (500 mg/kg/day) in their drinking water. Voluntary wheel running (i.e., voluntary running activity [VRA]) and grip strength were measured at Days 0, 8, 14, and 17 of tumor growth. Cardiac function was measured using echocardiography on Day 18 or 19. Biomarkers of inflammation, protein degradation, and oxidative stress were measured in serum and heart and gastrocnemius tissue.. VRA and grip strength progressively declined in tumor-bearing mice. Muscle mass and myocardial diastolic function were decreased, and expression of proinflammatory cytokines was increased in serum and muscle and heart tissue on Day 19 of tumor growth. Oxidative stress was present only in the heart, while biomarkers of protein degradation were increased only in the gastrocnemius muscle. Ubiquinol increased muscle mass in the tumor-bearing and control animals but had no effect on the expression of biomarkers of inflammation, protein degradation, or oxidative stress or on behavioral measures of fatigue. Topics: Adenocarcinoma; Animals; Antioxidants; Colonic Neoplasms; Fatigue; Female; Mice; Motor Activity; Muscle, Skeletal; Neoplasms, Experimental; Oxidative Stress; Ubiquinone | 2015 |
Coenzyme Q10 attenuated DMH-induced precancerous lesions in SD rats.
Coenzyme Q10 (CoQ10) is known to be a compound with mitochondrial bioenergetic functions and antioxidant activity. In this study, we evaluated the effect of CoQ10 on the formation of aberrant crypt foci (ACF) induced by 1,2-dimethylhydrazine (DMH), DMH-induced leukocytic DNA damage and gene expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) by real-time PCR in colonic mucosa of male SD rats. The animals were divided into three groups and fed a casein-based high-fat and low fiber diet (100 g lard+20 g cellulose/kg diet) with or without CoQ10 (0.4 mg in soybean oil/kg BW/d, i.p.). One week after beginning the diets, the rats were subjected to 6 wk of treatment with DMH (30 mg/kg/wk, s.c.) and CoQ10 treatments continued over the entirety of the experimental period (59 d). Administration of CoQ10 resulted in reduction of ACF numbers, to 20% of the carcinogen control value. CoQ10 supplementation induced an antigenotoxic effect on DMH-induced DNA damage in the blood cells. Colonic mucosa of DMH-injected rats had significantly greater COX-2 and iNOS gene expression than those of control rats, while treatment with CoQ10 induced an inhibitory effect on over-expression of COX-2 and iNOS in colon tumors. Our results provide evidence that CoQ10 has a protective effect on the process of colon carcinogenesis, suppressing the development of preneoplastic lesions, possibly by modulating COX-2 and iNOS gene expression in colonic mucosa and DNA damage in leukocytes, suggesting that CoQ10 has chemotherapeutic activity. Topics: 1,2-Dimethylhydrazine; Analysis of Variance; Animals; Anticarcinogenic Agents; Antioxidants; Colon; Colonic Neoplasms; Cyclooxygenase 2; DNA Damage; Intestinal Mucosa; Male; Nitric Oxide Synthase Type II; Precancerous Conditions; Rats; Rats, Sprague-Dawley; Reverse Transcriptase Polymerase Chain Reaction; Ubiquinone | 2010 |
Ubiquinol and the papaverine derivative caroverine prevent the expression of tumour- promoting factors in adenoma and carcinoma colon cancer cells induced by dietary fat.
High consumption of dietary fat promotes colon carcinogenesis. While this effect is well known the underlying mechanism is not understood. Fatty acid hydroperoxides (LOOH) arise from unsaturated fatty acids in the presence of oxygen and elevated temperature during food processing. An approach was made starting from the assumption that LOOH are present in dietary fats as a result of boiling. LOOH undergoes homolytic cleavage in the presence of iron. We studied their effects on gene expression in colorectal tumour cells using linoleic acid hydroperoxide (LOOH) as model compound. Addition to the medium of LT97 adenoma and SW480 carcinoma cells enhanced the production of hydrogen peroxide. Both cell lines were observed to increase VEGF and COX-II expression based on mRNA. Expression of VEGF was inhibited by caroverine and ubiquinon. Topics: Adenoma; Carcinoma; Colonic Neoplasms; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase Inhibitors; Dietary Fats; Gene Expression Regulation, Neoplastic; Humans; Linoleic Acids; Lipid Peroxides; Organic Chemicals; Pyrazoles; Quinoxalines; Sulfonamides; Tumor Cells, Cultured; Ubiquinone; Vascular Endothelial Growth Factor A | 2005 |
Indomethacin and ibuprofen preserve gastrocnemius muscle mass in mice bearing the colon-26 adenocarcinoma.
Skeletal muscle wasting is a prominent feature of cancer cachexia and involves decreased muscle protein synthesis and increased activity of the ubiquitin-proteasome pathway of protein degradation. We report that both indomethacin and ibuprofen improved body weight and weight of the gastrocnemius muscle in tumor-bearing mice. Ibuprofen increased the soluble protein content of the muscle without affecting muscle levels of phosphorylated p70 S6 kinase, a ribosomal kinase involved in protein synthesis. Paradoxically, indomethacin increased levels of ubiquitin-conjugated proteins. Further study is needed to understand the mechanism of action by which indomethacin and ibuprofen preserve body weight and muscle mass in the tumor-bearing mice. The data suggest that ibuprofen may have beneficial effects in the treatment of cancer cachexia. Topics: Adenocarcinoma; Animals; Anti-Inflammatory Agents, Non-Steroidal; Body Weight; Cachexia; Colonic Neoplasms; Disease Models, Animal; Female; Ibuprofen; Indomethacin; Mice; Muscle, Skeletal; Neoplasms, Experimental; Ubiquinone | 2004 |
Effects of immunostimulation with OK432, coenzyme Q10, or levamisole on dimethylhydrazine-induced colonic carcinogenesis in rats.
Effects of immunostimulation with OK432, Coenzyme Q10 (Co-Q10), or levamisole on dimethylhydrazine (DMH)-induced colonic carcinogenesis were investigated in 45 Donryu-rats. The manipulation with one of these immunopotentiators did not prevent DMH-induced colonic carcinogenesis in these rats. However, the number of tumors was significantly reduced and the incidence of invasive carcinomas decreased by immunostimulation. The treatment also reduced the number of lesions with epithelial dysplasia within the flat colonic mucosa. Topics: 1,2-Dimethylhydrazine; Animals; Biological Products; Cell Transformation, Neoplastic; Coenzymes; Colonic Neoplasms; Dimethylhydrazines; Epithelium; Intestinal Mucosa; Levamisole; Picibanil; Rats; Ubiquinone | 1986 |