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Objectives Pain associated with various underlying pathologies is a major cause of morbidity and diminished life quality in diabetic patients. Effective control of pain requires the use of analgesics with the best efficacy and with minimal side effects. Therefore, our aim in this study was to investigate the effects of non-steroidal anti-inflammatory drugs (NSAIDs) on pain in diabetic rats. Methods In this study, we investigated the analgesic effects of drugs belonging to three different classes of NSAIDs in a rat model of diabetes. Four diabetic groups received normal saline, diclofenac, piroxicam and ketorolac, respectively, and four non-diabetic groups received normal saline, diclofenac, piroxicam and ketorolac. Type 1 diabetes was induced in rats by a single injection of streptozotocin (60 mg/kg bw). Formalin (50 µL of 2.5%) nociception assay was used to examine the effect of treatment with diclofenac, piroxicam and ketorolac on acute and chronic pain in healthy and diabetic rats. Results Piroxicam showed significant analgesic effects both in the acute phase of pain (5–10 min after injection of formalin into the left hind paw), and in the chronic phase (20–60 min after formalin injection) in healthy as well as diabetic rats. Diclofenac and ketorolac also reduced pain scores in healthy rats. However, these two drugs failed to diminish pain in diabetic rats. Conclusion Our data point for better efficacy of piroxicam in controlling pain in diabetes.

Background and Aim Oxidative stress is the main factor in the development and progression of diabetes and its related complications. There is growing evidence that antioxidants supplementation can improve oxidative stress induced in diabetes. The present investigation was conducted to study the effects of Coenzyme Q10 (CoQ10) on the Oxidative Stress Index (OSI) in diabetic rats. Methods and Materials A total of 30 male rats were divided into five groups: saline, sesame oil (as a vehicle), CoQ10-treated (10 mg/kg/day), diabetic (induced with streptozotocin: 55 mg/kg), and CoQ10-treated diabetic (10 mg/kg/d). Then, we measured the Malondialdehyde (MDA), Total Oxidant Status (TOS), and Total Antioxidant Capacity (TAC) levels in the rats' liver homogenate. Additionally, the OSI was calculated. Ethical Considerations The Research Ethics Committee of Arak University of Medical Sciences approved this study (Code: IR.ARAKMU.REC.1397.119). Results results showed a significant decrease in the level of liver MDA (P=0.022), TOS (P=0.03), and OSI (P=0.028) in the CoQ10-treated diabetic group compared to the diabetic rats. No significant change was observed in the total thiol group (P=0.25) and TAC (P=0.77) level in diabetic rats' livers treated with CoQ10 compared to diabetic rats. Conclusion CoQ10 supplementation can reduce oxidative stress induced in the liver of diabetic rats through the suppression of TOS, OSI, and lipid peroxidation.

This paper is hypothesis letter and does not have abstract

Phenytoin as an anti-seizure medication, is useful for the prevention of tonic-clonic seizures and focal seizures. In this study we focused on the probable effects of Phenytoin drug on gene expression profile of liver related to lipid metabolism balance in mouse as a model. In this study, a group including 7 male mice of BALB/c were treated with phenytoin 3-5 mg/kg/day orally and a group including 7 male mice of BALB/c were took standard food. Liver tissue samples were isolated. Total RNA was extracted and cDNA was synthesized. Expression of Akt1, Leptin, Adipoq and GLUT4 genes was measured using Realtime RT-PCR method. Results showed an increase about 15 and 3 fold changes in Akt1 (P <0.001) and Adipoq (P <0.001) gene expression respectively in treatment group compare to control mice. Also, we detected decreasing in Leptin and GLUT4 genes expression in the mice treated with phenytoin drug. Several studies indicated that phenytoin can promote hyperglycemia in human and animal. We proposed here that this effects may resulted from an interference between the phenytoin drug and gene expression profile in liver. Decreasing of leptin level here may be a result of glucose level elevation in blood that can induce a satiety situation result in decrease of leptin production. It may that Akt1 gene expression is increased to compensate the low level of GLUT4 protein. We concluded that phenytoin is a relatively high-risk antiepileptic drug for obesity and metabolic syndrome, but more studies are needed.