Changes in gene expression of lactate carriers (MCT1 and CD147) in cardiac muscle of diabetic male rats: the effect of dichloroacetate and endurance training

Objective: Investigating the effect of green tea extract (GTE) on the testicular damage induced by cadmium chloride CdCl2 in male rats. Design: Randomized controlled study. Animals: 40 male Wistar rats. Procedures: Rats were randomly divided into four groups: A) control group (each rat daily received pellet diet); B) GTE group each rat daily received pellet diet as well as 3 ml of 1.5 % w/v GTE, C) CdCl2 group each rat was I/P injected a single dose of 1 mg/kg CdCl2, then daily received pellet diet, and D) CdCl2+GTE group each rat was I/P injected a single dose of 1 mg/kg CdCl2 then daily received pellet diet as well as 3 ml of 1.5 % w/v GTE. After 30 days, blood samples were collected for hormonal assays (testosterone, FSH, and LH). In addition, both testes were collected; one of them was used for quantification of 17-beta hydroxysteroid dehydrogenase III (17β-HSDIII) gene expression using a real-time PCR. The other testis was used for determination of catalase and reduced glutathione; GSH, Nitric oxide (NO) and malondialdehyde (MDA) levels. Results: CdCl2 decreased serum testosterone levels and its synthesis pathway (17β-HSDIII testicular gene expression). While antioxidants catalase and GSH were reduced, oxidants MDA were enriched in the testes of CdCl2-poisoned rats. This CdCl2-promoted testicular dysfunction was corrected via the administration of GTE to male rats. Conclusion and clinical relevance: GTE could be used as a remedy for protecting against CdCl2-induced testicular damage in male rats.

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The Protective Effect of Metformin against Oxandrolone-Induced Infertility in Male Rats

Current Pharmaceutical Design ◽

10.2174/1381612826666201029101524 ◽

2020 ◽

Vol 26 ◽

Author(s):

Abdulqader Fadhil Abed ◽

Yazun Bashir Jarrar ◽

Hamzeh J Al-Ameer ◽

Wajdy Al-Awaida ◽

Su-Jun Lee

Keyword(s):

Gene Expression ◽

Male Infertility ◽

Protective Effect ◽

Histological Examination ◽

Sperm Count ◽

Serum Testosterone ◽

Male Rats ◽

P Value ◽

Protective Effects ◽

Rt Pcr

Background: Oxandrolone is a synthetic testosterone analogue that is widely used among bodybuilders and athletes. However, oxandrolone causes male infertility. Recently, it was found that metformin reduces the risk of infertility associated with diabetes mellitus. Aim: This study aimed to investigate the protective effects of metformin against oxandrolone-induced infertility in male rats. Methods: Rats continuously received one of four treatments (n=7) over 14 days: control DMSO administration, oxandrolone administration, metformin administration, or co-administration of oxandrolone and metformin. Doses were equivalent to those used for human treatment. Subsequently, testicular and blood samples were collected for morphological, biochemical, and histological examination. In addition, gene expression of the testosterone synthesizing enzyme CYP11A1 was analyzed in the testes using RT-PCR. Results: Oxandrolone administration induced male infertility by significantly reducing relative weights of testes by 48%, sperm count by 82%, and serum testosterone levels by 96% (ANOVA, P value < 0.05). In addition, histological examination determined that oxandrolone caused spermatogenic arrest which was associated with 2-fold downregulation of testicular CYP11A1 gene expression. However, co-administration of metformin with oxandrolone significantly ameliorated toxicological alterations induced by oxandrolone exposure (ANOVA, P value < 0.05). Conclusion: Metformin administration protected against oxandrolone-induced infertility in male rats. Further clinical studies are needed to confirm the protective effect of metformin against oxandrolone-induced infertility among athletes.

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Effect of combination of peripheral oxytocin and naltrexone at subthreshold doses on food intake, body weight and feeding-related brain gene expression in male rats

Physiology & Behavior ◽

10.1016/j.physbeh.2021.113464 ◽

2021 ◽

pp. 113464

Author(s):

Mitchell A. Head ◽

Allen S. Levine ◽

David G. Christian ◽

Anica Klockars ◽

Pawel K. Olszewski

Keyword(s):

Gene Expression ◽

Body Weight ◽

Food Intake ◽

Male Rats ◽

Brain Gene Expression

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Endurance Training Regulates Expression of Some Angiogenesis-Related Genes in Cardiac Tissue of Experimentally Induced Diabetic Rats

Biomolecules ◽

10.3390/biom11040498 ◽

2021 ◽

Vol 11 (4) ◽

pp. 498

Author(s):

Mojdeh Khajehlandi ◽

Lotfali Bolboli ◽

Marefat Siahkuhian ◽

Mohammad Rami ◽

Mohammadreza Tabandeh ◽

...

Keyword(s):

Gene Expression ◽

Endurance Training ◽

Molecular Mechanisms ◽

Cardiac Tissue ◽

Critical Role ◽

Diabetic Rats ◽

Moderate Intensity ◽

Pcr Analysis ◽

Cardiac Tissues ◽

The Impact

Exercise can ameliorate cardiovascular dysfunctions in the diabetes condition, but its precise molecular mechanisms have not been entirely understood. The aim of the present study was to determine the impact of endurance training on expression of angiogenesis-related genes in cardiac tissue of diabetic rats. Thirty adults male Wistar rats were randomly divided into three groups (N = 10) including diabetic training (DT), sedentary diabetes (SD), and sedentary healthy (SH), in which diabetes was induced by a single dose of streptozotocin (50 mg/kg). Endurance training (ET) with moderate-intensity was performed on a motorized treadmill for six weeks. Training duration and treadmill speed were increased during five weeks, but they were kept constant at the final week, and slope was zero at all stages. Real-time polymerase chain reaction (RT-PCR) analysis was used to measure the expression of myocyte enhancer factor-2C (MEF2C), histone deacetylase-4 (HDAC4) and Calmodulin-dependent protein kinase II (CaMKII) in cardiac tissues of the rats. Our results demonstrated that six weeks of ET increased gene expression of MEF2C significantly (p < 0.05), and caused a significant reduction in HDAC4 and CaMKII gene expression in the DT rats compared to the SD rats (p < 0.05). We concluded that moderate-intensity ET could play a critical role in ameliorating cardiovascular dysfunction in a diabetes condition by regulating the expression of some angiogenesis-related genes in cardiac tissues.

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Early maternal deprivation impairs learning and memory and alters hippocampal gene expression in adult male rats

Neurobiology of Learning and Memory ◽

10.1016/j.nlm.2021.107479 ◽

2021 ◽

pp. 107479

Author(s):

Xiaofan Xiong ◽

Lin Han ◽

Meiyang Fan ◽

Lingyu Zhang ◽

Liying Liu ◽

...

Keyword(s):

Gene Expression ◽

Learning And Memory ◽

Adult Male ◽

Maternal Deprivation ◽

Male Rats

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Stress Modifies the Expression of Glucocorticoid-Responsive Genes by Acting at Epigenetic Levels in the Rat Prefrontal Cortex: Modulatory Activity of Lurasidone

International Journal of Molecular Sciences ◽

10.3390/ijms22126197 ◽

2021 ◽

Vol 22 (12) ◽

pp. 6197

Author(s):

Paola Brivio ◽

Giulia Sbrini ◽

Letizia Tarantini ◽

Chiara Parravicini ◽

Piotr Gruca ◽

...

Keyword(s):

Gene Expression ◽

Dna Methylation ◽

Chronic Stress ◽

Chronic Mild Stress ◽

Male Rats ◽

Mild Stress ◽

Experimental Conditions ◽

Glucocorticoid Responsive Element ◽

Responsive Element

Epigenetics is one of the mechanisms by which environmental factors can alter brain function and may contribute to central nervous system disorders. Alterations of DNA methylation and miRNA expression can induce long-lasting changes in neurobiological processes. Hence, we investigated the effect of chronic stress, by employing the chronic mild stress (CMS) and the chronic restraint stress protocol, in adult male rats, on the glucocorticoid receptor (GR) function. We focused on DNA methylation specifically in the proximity of the glucocorticoid responsive element (GRE) of the GR responsive genes Gadd45β, Sgk1, and Gilz and on selected miRNA targeting these genes. Moreover, we assessed the role of the antipsychotic lurasidone in modulating these alterations. Chronic stress downregulated Gadd45β and Gilz gene expression and lurasidone normalized the Gadd45β modification. At the epigenetic level, CMS induced hypermethylation of the GRE of Gadd45β gene, an effect prevented by lurasidone treatment. These stress-induced alterations were still present even after a period of rest from stress, indicating the enduring nature of such changes. However, the contribution of miRNA to the alterations in gene expression was moderate in our experimental conditions. Our results demonstrated that chronic stress mainly affects Gadd45β expression and methylation, effects that are prolonged over time, suggesting that stress leads to changes in DNA methylation that last also after the cessation of stress procedure, and that lurasidone is a modifier of such mechanisms.

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