ABSTRACT
Several studies point to an important function of cyclooxygenase [COX] and prostaglandin signaling in models of synaptic plasticity which is associated with W-methyl-D-aspartate receptors [NMDARs]. Cyclooxygenase gene is suggested to be an immediate early gene that is tightly regulated in neurons by NMD A dependent synaptic activity. Nonsteroid Antiinflammatory Drugs [NSAIDs] exert their antiinflammatory effect by the inhibion of COX have controversial effects on learning and memory. We administered ibuprofen as a non-selective COX-2 inhibitor and nimesulide as a selective COX-2 inhibitor for 8 weeks for determining the cognitive impact of subchronic administration of NSAIDs to aged rats. Wistar albino rats [16 mo, n = 30] were separated into control [n = 10], ibuprofen [n = 10] and nimesulide [n = 10] treated groups. First we evaluated hippocampus-dependent spatial memory in the radial arm maze [RAM] and than we evaluated the expression of the NMDAR subunits, NR2A and NR2B by western blotting to see if their expressions are effected by subchronic administration with these drugs. Ibuprofen and nimesulide treated rats completed the task in a statistically significant shorter time when compared with control group [p < 0.01], but there was no statistically significant difference between groups about choice accuracy data in RAM. Furthermore, no statistically significant difference was detected for the protein expressions of NR2A and NR2B of the subjects. Oral administration of ibuprofen and nimesulide for 8 weeks showed no impairment but partly improved spatial memory
ABSTRACT
Because subclinical thyroid dysfunction may be a risk factor for cardiovascular disease, we evaluated the atherosclerosis tendency in subclinical hypothyroid [SCH] patients. Fifty-three subclinical hypothyroid patients [serum thyrotropin [TSH] concentrations >4.12 mU/L] were compared with a control group of 50 euthyroid subjects whose age, sex and body mass indices were similar to the patient group. We tested whether serum TSH concentrations were correlated with plasma total homocysteine concentration [tHcy], low-density lipoprotein cholesterol [LDL-C], very low-density lipoprotein cholesterol [VLDL-C], high-density lipoprotein cholesterol [HDL-C], total cholesterol [TC] and triglycerides [TG]. There was a significant statistical difference between the patient and control groups for normal freeT4 [1.02 +/- 0.1 7 vs. 0.86 +/- 0.13, P<.001], TSH [1.64 +/- 1.02 vs. 6.62 +/- 2.61, P<.001], TC [1 85 +/- 39 vs. 206 +/- 42, P=.01], TG [103 +/- 54 vs. 132 +/- 85, P=.04], LDL-C [114 +/- 33 vs. 127 +/- 36, P=.04], and TC/HDL-C [3.81 +/- 106 vs. 4.19 +/- 1.02, P=.04], respectively. No statistically significant difference was found between the two groups for HDL-C, VLDL-C, LDL-C/HDL-C, and tHcy. Serum TSH was significantly correlated with plasma tHcy [r=0.55; P=.001], TC [r=0.52; P=.001], LDL-C [r=0.49; P=.001], TC/HDL-C [r=0.38; P=.002] and LDL-C/HDL-C [r=0.36; P=.004] across all participants. Our study suggests that the atherogenicity of SCH is not mediated by hyperhomocysteinemia. Associated hyperlipidemia may explain the observed increased risk of coronary artery disease in patients with SCH