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Mousavi S.E.,Shahid Chamran University | Shahriari A.,Shahid Chamran University | Ahangarpour A.,Jundishapour Medical science University | Vatanpour H.,Shahid Chamran University | Jolodar A.,Shahid Beheshti University
Iranian Journal of Pharmaceutical Research | Year: 2012

Possessing putative hypolipidemic effects, Teucrium polium (TP) have been traditionally used as a medicinal plant in Iran. The aim of the present study was to investigate this effect on the sucrose-induced insulin resistance male rat model. Thirty Wistar male rats weighting 180 ± 20 g were divided into five groups of six each. Four groups were given sucrose 50% in drinking water for 10 weeks. In 8th week of treatment, three groups of them were randomly selected and treated with Teucrium polium (T. polium) ethyl acetate extract (50, 100 and 200 mg/Kg for two weeks). Control animals were fed using normal rat chow. After ten weeks, blood samples were collected from the heart. Blood Glucose, insulin, leptin, lipid content and fasting insulin resistance index (FIRI) as well as liver and muscle glycogen and lipid contents were determined. Final data were analyzed by ANOVA and post-hoc Tukey's test. Liver glycogen contents and blood levels of glucose and insulin were significantly increased in high sucrose (HS) group compared with control group. A significant decrease was observed in blood glucose and insulin levels, FIRI, serum total lipid, triglyceride and VLDL-c as well as the liver triglyceride level, muscle and liver glycogen contents in 100 and 200 mg/Kg of TP-treated groups compared with HS group. Leptin level was significantly decreased in 50 and 100 mg/Kg groups compared with HS group. The treatment with T. polium ethyl acetate extract (TP-EAE) induced a dose-dependent reduction in serum, liver and muscle triglyceride (TG) and liver glycogen content levels, as well as serum insulin. These effects may be attributed, in part, to the hypolipidemic effect of TP flavonoids; otherwise, the hepatoprotective and antioxidant activity of TP-EAE may improve the liver function and reverse harmful sucrose effects. © 2012 by School of Pharmacy.

Ashabi G.,Jundishapour Medical science University | Khalaj L.,Alborz University of Medical Science | Khodagholi F.,Shahid Beheshti University of Medical Sciences | Goudarzvand M.,Alborz University of Medical Science | Sarkaki A.,Jundishapour Medical science University
Metabolic Brain Disease | Year: 2015

Global cerebral ischemia arises in patients who have a variety of clinical conditions including cardiac arrest, shock and asphyxia. In spite of advances in understanding of the brain ischemia and stroke etiology, therapeutic approaches to improve ischemic injury still remain limited. It has been established that metformin can attenuate cell death in cerebral ischemia. One of the main functions of metformin is proposed to be conducted via AMP-activated protein kinase (AMPK)-dependent pathway in the experimental cerebral ischemia model. It is also established that metformin can suppress inflammation and activate Nuclear factor erythroid 2-related factor (Nrf2) pathways in neurons. In the current study, the role of metformin in regulating inflammatory and antioxidant pathways in the global cerebral ischemia was investigated. Our results indicated that pretreatment of rats by metformin attenuated cellular levels of nuclear factor-κB, Tumor Necrosis Factor alpha and Cyclooxygenase-2 which are considered as three important proteins involved in the inflammation pathway. Pretreatment by metformin increased the level of Nrf2 and heme oxygenase-1 in the hippocampus of ischemic rats compared with untreated ischemic group. Moreover, pretreatment by metformin enhanced the level of glutathione and catalase activities compared with them in ischemic group. Such protective changes detected by metformin pretreatment were reversed by injecting compound c, an AMPK inhibitor. These findings suggested that metformin might protect cells through modulating inflammatory and antioxidant pathways via induction of AMPK. However, more experimental and clinical trial studies regarding neuroprotective potential of metformin and the involved mechanisms, especially in the context of cerebral ischemic injuries, are necessary. © 2014, Springer Science+Business Media New York.

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