No abstract

No abstract

No abstract

Objective: In the last two decades, research on epigenetic mechanisms has expanded dramatically. Recent studies demonstrated that epigenetic mechanisms regulate epilepsy and epileptogenic pathologies. In this study, we aimed to investigate changes in the promoter methylation status of the voltage-gated T-type calcium channel alpha 1 subunit G (CACNA1G) gene and total histone deacetylase activity in Wistar Albino Glaxo/Rijswijk (WAG/Rij) rats which is one of the commonly used genetic absence rat models of epilepsy in the three different age groups (3, 6, and 9 months old) on both sexes. Material and Method: Evaluation of changes in the spike-wave discharges (SWDs) was performed with electrocorticography (ECoG). The promoter methylation status of the CACNA1G gene was determined by methylation-specific PCR (MSP), and histone deacetylase (HDAC) activity was determined spectrophotometrically. Results: Our results demonstrated that the number of SWDs increased time-dependent in WAG/Rij. Additionally, it was observed that CACNA1G promoter methylation decreased, and total HDAC activity increased with age in both sexes. Conclusion: Our results provide further support for epigenetic regulation in the absence epilepsy phenotype and suggest that the underlying mechanism behind the increase in the number of SWDs with age in the WAG/Rij animals might be regulated by CACNA1G promoter methylation or HDAC activity.

Rilmenidine protects against joint damage in MIA-induced model of osteoarthritis in rats Purpose: Osteoarthritis is a common problem, and its incidence significantly increases with age. Patients suffer from excruciating pain while moving, and currently, major treatment options consist of surgery. Rilmenidine is a potent antihypertensive agent with a high affinity for imidazoline and alpha2 adrenergic receptors. Based on the knowledge that these receptors are also related to bone turnover and pain, we aimed to reveal the effect of rilmenidine on the osteoarthritis model in rats. Methods: Monosodium iodoacetate(MIA) was used to induce osteoarthritis. Animals were treated with rilmenidine(0.5, 2 mg/kg) for 14 days. Hot plate test was performed to assess pain response before and end of the drug treatments, in addition to the walking track analysis. Twenty-four hours after the last drug treatment, serum levels of receptor activator of nuclear factor kappa-Β ligand(RANKL) and osteoprotegerin(OPG) were measured. Hematoxylin&eosin and safranin-O staining were used to evaluate MIA and rilmenidine induced changes in the hindlimb joints. Results: Our results demonstrated that rilmenidine(2 mg/kg) prevented MIA-induced thermal hyperalgesia with improved walking behavior in the walking track test. Additionally, rilmenidine(2 mg/kg) also prevented MIA-induced increase in the RANKL and OPG levels in the serum. Histopathological analysis showed that rilmenidine was protective on joint capsule and matrix. Conclusion: Our results suggest that rilmenidine showed the antinociceptive effect on MIA-induced OA via improving bone turnover.