Chemopreventive effect of spirulina microalgae on an animal model of glioblastoma via down‐regulation of PI3K / AKT / mTOR and up‐regulation of miR ‐34a/ miR‐125B expression

2021 ◽  
Author(s):  
Samaneh Arab ◽  
Sahar Ghasemi ◽  
Ali Ghanbari ◽  
Marjan Bahraminasab ◽  
Atefeh Satari ◽  
...  
Keyword(s):  
Animal Model ◽  
Down Regulation ◽  
Chemopreventive Effect

scholarly journals Gene Expression and DNA Methylation Alterations in the Glycine N-Methyltransferase Gene in Diet-Induced Nonalcoholic Fatty Liver Disease-Associated Carcinogenesis

2019 ◽  
Vol 170 (2) ◽  
pp. 273-282 ◽  
Author(s):  
Barbara Borowa-Mazgaj ◽  
Aline de Conti ◽  
Volodymyr Tryndyak ◽  
Colleen R Steward ◽  
Leandro Jimenez ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Animal Model ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
The United States ◽  
Down Regulation ◽  
Nonalcoholic Fatty Liver

Abstract Nonalcoholic fatty liver disease (NAFLD) is becoming a major etiological risk factor for hepatocellular carcinoma (HCC) in the United States and other Western countries. In this study, we investigated the role of gene-specific promoter cytosine DNA methylation and gene expression alterations in the development of NAFLD-associated HCC in mice using (1) a diet-induced animal model of NAFLD, (2) a Stelic Animal Model of nonalcoholic steatohepatitis-derived HCC, and (3) a choline- and folate-deficient (CFD) diet (CFD model). We found that the development of NAFLD and its progression to HCC was characterized by down-regulation of glycine N-methyltransferase (Gnmt) and this was mediated by progressive Gnmt promoter cytosine DNA hypermethylation. Using a panel of genetically diverse inbred mice, we observed that Gnmt down-regulation was an early event in the pathogenesis of NAFLD and correlated with the extent of the NAFLD-like liver injury. Reduced GNMT expression was also found in human HCC tissue and liver cancer cell lines. In in vitro experiments, we demonstrated that one of the consequences of GNMT inhibition was an increase in genome methylation facilitated by an elevated level of S-adenosyl-L-methionine. Overall, our findings suggest that reduced Gnmt expression caused by promoter hypermethylation is one of the key molecular events in the development of NAFLD-derived HCC and that assessing Gnmt methylation level may be useful for disease stratification.

Duodenal Reflux Leads to Down Regulation of DNA Mismatch Repair Pathway in an Animal Model of Esophageal Cancer

2007 ◽  
Vol 83 (2) ◽  
pp. 433-440 ◽  
Author(s):  
Pramod Bonde ◽  
Daqing Gao ◽  
Lei Chen ◽  
Tomoharu Miyashita ◽  
Elizabeth Montgomery ◽  
...  
Keyword(s):  
Animal Model ◽  
Esophageal Cancer ◽  
Mismatch Repair ◽  
Dna Mismatch Repair ◽  
Repair Pathway ◽  
Down Regulation ◽  
Dna Mismatch ◽  
Mismatch Repair Pathway ◽  
Duodenal Reflux

P–075 HAART exacerbates anti-Koch-induced reproductive toxicity via suppression of androgen and down-regulation of cGMP signaling

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
M Hamed ◽  
R Akhigbe
Keyword(s):  
Animal Model ◽  
Dehydrogenase Activity ◽  
Sexual Behaviour ◽  
Sperm Quality ◽  
Reproductive Toxicity ◽  
Reproductive Function ◽  
Antiretroviral Drugs ◽  
Down Regulation ◽  
Cgmp Signaling ◽  
The Impact

Abstract Study question Will highly active antiretroviral drugs (HAART) and antikochs impair reproductive function when used singly and concurrently? Summary answer HAART exacerbates antikoch-induced reproductive toxicity by stimulating testicular and penile oxido-inflammatory response. This was associated with suppression of androgen and down-regulation of cGMP signaling. What is known already Although the advent of HAART and antikochs has significantly improved the clinical status, life expectancy and quality of life of patients with HIV/tuberculosis, these drugs are with shortcomings. Studies have reported that HAART induces testicular toxicity and impairs sperm quality. Similarly, antikochs has been shown to trigger oxidative testicular and sperm damage. Available data have implicated HAART and antikoch in the pathogenesis of male infertility via oxidative stress-mediated mechanism. However, no study has reported the impact of the concurrent administration of both HAART and antikochs as seen in patients with TB/HIV co-infection on testicular function, sexual behaviour and fertility outcome. Study design, size, duration This is a prospective experimental study using animal model. Forty sexually mature inbred male Wistar rats of comparable age were used for the study. The study lasted 8 weeks. Participants/materials, setting, methods Animals were acclimatized for two weeks after which they were randomly allotted into four groups (n = 10). The control rats 0.5mL of distilled water as vehicle, anti-Koch-treated rats received a cocktail of anti-tuberculosis drugs (Rifampicin, Isoniazid, Pyrazinamide, and Ethambutol), HAART-treated animals received a cock-tail of antiretroviral drugs (Efavirenz, Lamivudine, and Tenofovir), while the HAART+antikochs-treated rats received treatment as HAART-treated as well as antikoch-treated. The doses of drugs used were the Human Equivalent doses for rats. Main results and the role of chance HAART exaggerated antikoch-induced increase in testicular lactate dehydrogenase activity, concentrations of lactate and uric acid, and reduced testicular sorbitol dehydrogenase activity. Furthermore, HAART worsens antikoch-induced decline in the activities of testicular and penile superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase, as well as glutathione concentration, but increased malondialdehyde levels in testicular and penile tissues, as well as penile and testicular DNA fragmentation. Similarly, HAART aggravates antikoch-driven reduction in penile cGMP, circulatory and testicular testosterone, serum prolactin, LH and FSH, impaired sperm quality, sexual behaviour, and fertility outcome. Limitations, reasons for caution This is a prospective study using animal model; hence findings should be extrapolated to human with care. Human studies are thus recommended. Wider implications of the findings: This study demonstrates for the first time the impact of HAART and antikoch, when used singly or in combination, on sexual behaviour, sperm quality and penile and testicular integrity. The findings add to the available literature by providing the molecular mechanism through which HAART and/or antikoch possibly impair reproductive function. Trial registration number N/A

P541 QUERCETIN INDUCES HSC APOPTOSIS, UP-REGULATION OF CB2 AND DOWN-REGULATION OF CB1 IN AN ANIMAL MODEL OF LIVER FIBROSIS

2014 ◽  
Vol 60 (1) ◽  
pp. S250
Author(s):  
L. Hernandez Ortega ◽  
A.A. Sobrevilla Navarro ◽  
A.M.M. Salazar Montes ◽  
J. Armendariz-Borunda
Keyword(s):  
Animal Model ◽  
Liver Fibrosis ◽  
Down Regulation
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