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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.

Objective: Aspartame is a widely used artificial sweetener that was approved by the United States Food and Drug Administration (FDA) in 1996 for use as a general sweetener in all foods. Previous studies on aspartame had suggested it to be non-toxic. However, some studies have reported it to have carcinogenic, neurotoxic, apoptotic, and inflammatory effects. The knowledge obtained from previous studies has been insufficient and contradictory, thus the aim of this study was to demonstrate the harmful side effects of daily and high doses of aspartame on the rat livers. Materials and Methods:The study separated 18 Long Evans rats weighing between 250-300g into three groups: control, low dosage, and high dosage groups (n = 6 in each). 50 mg/kg of aspartame was given to the low dose group and 250 mg/kg to the high dose group every day for 10 weeks. At the end of the 10 th week, all groups were euthanized and their livers and blood samples collected. Liver tissues were subjected to hematoxylin-eosin and Masson's trichome staining, after which terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) immunohistochemistry was performed to check the serum alanine transaminase (ALT) and aspartate transaminase (AST) values. The enzymelinked immunosorbent assay (ELISA) method was applied for analyzing superoxide dismutase (SOD) and malondialdehyde (MDA) levels.Results: Enlargement of the bile canaliculi and dilatation of sinusoids were observed in the group that was given high doses of aspartame. At the same time, the amount of TUNEL-positive cells was higher in the high dose group. AST, ALT, and MDA values were increased while SOD values were decreased in both the low and high aspartame dosage groups. Conclusion:This study has concluded the prolonged use of high doses of aspartame to be able to cause damage to hepatocytes by stimulating oxidative stress, hepatocyte apoptosis, and necrosis.