Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add filters








Language
Year range
1.
The Korean Journal of Physiology and Pharmacology ; : 257-267, 2018.
Article in English | WPRIM | ID: wpr-728616

ABSTRACT

The present study aimed to evaluate the cinnamic acid effect on memory impairment, oxidative stress, and cholinergic dysfunction in streptozotocin (STZ)-induced diabetic model in mice. In this experimental study, 48 male Naval Medical Research Institute (NMRI) mice (30–35 g) were chosen and were randomly divided into six groups: control, cinnamic acid (20 mg/kg day, i.p. ), diabetic, and cinnamic acid-treated diabetic (10, 20 and 40 mg/kg day, i.p. ). Memory was impaired by administering an intraperitoneal STZ injection of 50 mg/kg. Cinnamic acid was injected for 40 days starting from the 21st day after confirming STZ-induced dementia to observe its therapeutic effect. Memory function was assessed using cross-arm maze, morris water maze and passive avoidance test. After the administration, biochemical parameters of oxidative stress and cholinergic function were estimated in the brain. Present data indicated that inducing STZ caused significant memory impairment, whereas administration of cinnamic acid caused significant and dose-dependent memory improvement. Assessment of brain homogenates indicated cholinergic dysfunction, increase in lipid peroxidation and reactive oxygen species (ROS) levels, and decrease in glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities in the diabetic group compared to the control animals, whereas cinnamic acid administration ameliorated these indices in the diabetic mice. The present study demonstrated that cinnamic acid improves memory by reducing the oxidative stress and cholinergic dysfunction in the brain of diabetic mice.


Subject(s)
Animals , Humans , Male , Mice , Academies and Institutes , Brain , Catalase , Dementia , Glutathione , Lipid Peroxidation , Memory Disorders , Memory , Oxidative Stress , Reactive Oxygen Species , Streptozocin , Superoxide Dismutase , Water
2.
Gastroenterology and Hepatology from Bed to Bench. 2017; 10 (1): 44-53
in English | IMEMR | ID: emr-185420

ABSTRACT

Aim: The aim of the present study was to evaluate the different doses of Butyric acid [BA] and Arsenic [As] in liver mitochondria oxidative stress and pancreatic islet insulin secretion of male mouse


Background: BA is found in many foods and As as a toxic metal is present in drinking water. They can induce oxidative stress in tissues


Methods: In this experimental study, Liver mitochondria were isolated by administration of the different centrifugation method and pancreatic islets were isolated by collagenase method. Mitochondria were incubated by BA [35, 75, 150, 300 microM] and As [20, 50, 100, 200 microM] as the islets were incubated by BA [250, 500, 1000, 1500 microM] and As [50, 100, 200 microM] for 1 hour. At the end of the experiment, mitochondrial viability and membrane potential, ROS, MDA, GSH and islets insulin secretion were measured by their specific methods


Results: BA and As administration increased mitochondrial levels of ROS, MDA and decreased GSH and pancreatic islet insulin secretion in a dose dependent manner [p<0.05]. The doses of BA 75microM and As 100microM have been revealed the most mitochondria toxic concentrations. Also, the doses of 1000microM for BA and 100microM for As were considered as reducing concentrations for islets insulin secretion. Additionally, co administration of them intensified more these effects


Conclusion: Alone or in combination administration of BA and As induced oxidative stress in liver mitochondria and decreased insulin secretion of pancreatic islets

SELECTION OF CITATIONS
SEARCH DETAIL