Publications by authors named "Jafar Doost Mohammadpour"

2 Publications

  • Page 1 of 1

Alterations in Plasma Glucose and Cardiac Antioxidant Enzymes Activity in Streptozotocin-Induced Diabetic Rats: Effects of Trigonella foenum-graecum Extract and Swimming Training.

Can J Diabetes 2016 Apr 6;40(2):135-42. Epub 2016 Jan 6.

Department of Physiology, Faculty of Medicine, Ilam University of Medical Sciences, Ilam, Iran.

Objectives: Diabetes mellitus is a group of metabolic diseases characterized by chronic hyperglycemia. Trigonella foenum-graecum (fenugreek) and swimming training have previously been reported to have hypoglycemic and antioxidant effects. We aimed to evaluate the effects of swimming training and fenugreek aqueous extract, alone and in combination, on plasma glucose and cardiac antioxidant enzymes activity of streptozotocin-induced diabetes in rats.

Methods: We divided 70 male Wistar rats equally into 7 groups: diabetic control (DC), healthy control (HC), swimming (S), fenugreek seed extract (1.74 g/kg) (F1), fenugreek seed extract (0.87 g/kg) (F2), swimming + fenugreek seed extract (1.74 g/kg) (SF1), and swimming + fenugreek seed extract (0.87 g/kg) (SF2). We used streptozotocin for the induction of diabetes. Statistical analyses were performed using the statistical program SPSS.

Results: We did not detect any significant differences in body weight in the F1, F2, S, SF1 and SF2 groups compared with the DC group (p>0.05). The results also revealed that the hypoglycemic effect of combined swimming and fenugreek was significantly stronger (p<0.05) than either of those alone. The F1, S, SF1 and SF2 groups showed improved superoxide dismutase activity with respect to the DC group (p<0.05). Catalase activity in the F1, S, SF1 and SF2 groups were significantly higher than those of the DC group (p<0.05). Glutathione peroxidase activity in the S, SF1 and SF2 groups were significantly increased compared with the DC group (p<0.05).

Conclusions: Our findings suggest that the combination of fenugreek seed extract and swimming could be useful for the treatment of hyperglycemia and cardiac oxidative stress induced by type 1 diabetes mellitus.
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http://dx.doi.org/10.1016/j.jcjd.2015.08.012DOI Listing
April 2016

Non-selective NSAIDs improve the amyloid-β-mediated suppression of memory and synaptic plasticity.

Pharmacol Biochem Behav 2015 05 17;132:33-41. Epub 2015 Feb 17.

Department of Physiology and Pharmacology, Qom University of Medical Sciences and Health Services, Qom, Iran.

Alzheimer's disease (AD) is characterized by the formation of amyloid beta (Aβ) plaques in the brain. Dysfunctional excitatory synaptic transmission and neuronal plasticity are generally accepted as primary events in the development of AD. There is evidence to suggest that both COX-1 expression and COX-2 expression are changed in the brain of AD patients. However, the impact of COX-dependent mechanisms on synaptic dysfunction underlying the memory deficit is not fully elucidated. In the present study effects of non-selective NSAIDs (aspirin and sodium salicylate) on associated memory impairment as well as Aβ-mediated suppression of synaptic plasticity in the hippocampus were examined. Aβ1-42 (5μg/μl) and ibotenic acid (5μg/μl) were injected bilaterally into the dorsal hippocampus of rats and the spatial memory and long term potentiation (LTP) were assessed by water maze performance and in vivo field potential recording, respectively. Field excitatory post synaptic potentials (fEPSP) were recorded from stratum radiatum of area CA1 following Schaffer collateral stimulation. Behavioral study revealed that both sub-chronic high dose of sodium salicylate (SS) and chronic low dose of aspirin improved the spatial memory impairment of Aβ treated rats, however the effects of SS were lower than those of aspirin. Animals treated with SS and aspirin showed a significant decrease in escape latency (SS: F(1, 24)=15.85, p<0.01, aspirin: F(1, 22)=25.24, p<0.001, ANOVA). Furthermore, in probe test, animals treated with aspirin (p<0.05) but not SS (p>0.05) spent more time (one-way ANOVA) in target quadrant zone. Both applied drugs restored the suppression of fEPSP slope LTP that was induced by Aβ treatment (unpaired t-test, p<0.001). Aspirin showed a preventative effect also against Aβ-induced changes in LTP and memory task when applied before Aβ administration. Since aspirin and SS improved synaptic dysfunction, we can suggest that COX-dependent mechanisms may play a role in synaptic dysfunction in an experimental model of AD.
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http://dx.doi.org/10.1016/j.pbb.2015.02.012DOI Listing
May 2015