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Showing 2 results for Baluchnejadmojarad

M Roghani, T Baluchnejadmojarad, M Fallah_ Mohammadi,
Volume 15, Issue 59 (6-2007)
Abstract

Background and Objective: Diabetes mellitus (DM) especially type A, is accompanied by disturbances in learning, memory, and cognitive skills in human society and experimental animals. Regarding the beneficial effect of SM on lipid peroxidation in hyperlipidemia and on serum lipids in DM, this study was conducted to evaluate the effect of prolonged oral administration of SM on learning and memory in diabetic rats. Materials and Methods: Female wistar rats (n = 36) were randomly divided into control, SM-treated control, diabetic, and SM-treated diabetic groups. Treatment groups received a mixture of SM and standard rat food at a weight ratio of 6.25% for 4 weeks.To induce diabetes, streptozotocin was injected intraperitoneally at a single dose of 60 mg/kg. For evaluation of learning and memory, initial latency (IL) and step-through latency (STL) were determined at the end of the study using passive avoidance test. Meanwhile, alternation behavior percentage was determined using Y maze test. Results: There was a significant increase (p = 0.032) in IL in diabetic and SM-treated diabetic groups after 4 weeks compared to control group. There was no significant difference between diabetic and SM-treated diabetic groups. On the other hand, STL decreased significantly (p = 0.032) in diabetic group while it increased significantly (p = 0.027) in SM-treated group compared to control group at the end of the study. The results of Y maze showed that alternation score was not different between treated and untreated diabetic groups. Conclusion: SM could enhance the consolidation and recall capability of stored information but did not affect spatial memory of diabetic animals.


T Baluchnejadmojarad, M Roghani, P Kazemloo,
Volume 25, Issue 113 (8-2017)
Abstract

Background and Objective: Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases and results from the extracellular accumulation of b-amyloid peptides and the resulting neuronal dysfunction. In this study, the role of nicotinic acetylcholine receptors, protein kinase B (PKB) and protein kinase M (PKM) were evaluated in order to examine the mechanism of the protective effects of rosmarinic acid in a rat model of Alzheimer’s disease.
Materials and Methods: Animals[vog1]  were divided into 6 groups consisting of 1) Sham, 2) Beta amyloid, 3) Rosmarinic acid pretreated beta amyloid (25 mg/kg), 4-6) Rosmarinic acid and PKM inhibitor, PKB inhibitor and acetylcholine receptor inhibitor pretreated beta amyloid. Two weeks post-surgery, behavioral (alternation percent in Y maze and step through latency in passive avoidance task) and histochemical (hippocampal malondialdehyde and neuronal density measurement) studies were performed.
Results: Pretreatment of beta amyloid animals with rosmarinic acid considerably alleviated the behavioral and histochemical disturbances related to the hippocampus. In this group, nicotinic acetylcholine receptors and PKB inhibitors decreased step through latency (p<0.001) and increased hippocampal malondialdehyde levels (p<0.001). In addition, PKB inhibitors decreased hippocampal neuronal density in rosmarinic acid pretreated beta amyloid rats (p<0.05).
Conclusion: Based on the findings of this study, it seems that in this experimental model of Alzheimer’s disease the protective effects of rosmarinic acid were derived from its antioxidant properties and partially via nicotinic acetylcholine receptors, PKB and PKM.

 [vog1]Which animals??
How many???


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