Novel role for gabapentin in neuroprotection of central nervous system in streptozotocine-induced diabetic rats1

Baydaş, Gıyasettin; Sonkaya, Ertuğrul; Tuzcu, Mehmet; Yasar, Abdullah; Dönder, Emir

doi:10.1111/j.1745-7254.2005.00072.x

Cited by 51 publications

(44 citation statements)

References 32 publications

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“…These results confirmed the previous reports that streptozotocin-induced diabetes was accompanied by an increased generation of reactive species. It is also suggested that the antioxidant compounds may have beneficial effects against the complications of diabetes mellitus [34–36]. …”

Section: Discussionmentioning

confidence: 99%

Beneficial Effects ofTeucrium poliumand Metformin on Diabetes-Induced Memory Impairments and Brain Tissue Oxidative Damage in Rats

Mousavi

Niazmand

Hosseini

et al. 2015

International Journal of Alzheimer's Disease

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Objective. The effects of hydroalcoholic extract of Teucrium polium and metformin on diabetes-induced memory impairment and brain tissues oxidative damage were investigated. Methods. The rats were divided into: (1) Control, (2) Diabetic, (3) Diabetic-Extract 100 (Dia-Ext 100), (4) Diabetic-Extract 200 (Dia-Ext 200), (5) Diabetic-Extract 400 (Dia-Ext 400), and (6) Diabetic-Metformin (Dia-Met). Groups 3–6 were treated by 100, 200, and 400 mg/kg of the extract or metformin, respectively, for 6 weeks (orally). Results. In passive avoidance test, the latency to enter the dark compartment in Diabetic group was lower than that of Control group (P < 0.01). In Dia-Ext 100, Dia-Ext 200, and Dia-Ext 400 and Metformin groups, the latencies were higher than those of Diabetic group (P < 0.01). Lipid peroxides levels (reported as malondialdehyde, MDA, concentration) in the brain of Diabetic group were higher than Control (P < 0.001). Treatment by all doses of the extract and metformin decreased the MDA concentration (P < 0.01). Conclusions. The results of present study showed that metformin and the hydroalcoholic extract of Teucrium polium prevent diabetes-induced memory deficits in rats. Protection against brain tissues oxidative damage might have a role in the beneficial effects of the extract and metformin.

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Section: Discussionmentioning

confidence: 99%

Beneficial Effects ofTeucrium poliumand Metformin on Diabetes-Induced Memory Impairments and Brain Tissue Oxidative Damage in Rats

Mousavi

Niazmand

Hosseini

et al. 2015

International Journal of Alzheimer's Disease

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“…These studies support increased MDA levels during diabetes and protective effects of bosentan. The increase in lipid peroxidation, on the other hand, leads to a decrease in a very important endogenous antioxidant substance, like glutathione [64,65]. Glutathione was found to be low in the diabetic rat groups in our study.…”

Section: Discussionmentioning

confidence: 70%

Does Bosentan Protect Diabetic Brain Alterations in Rats? The Role of Endothelin‐1 in the Diabetic Brain

Demir

Çadırcı

Akpınar

et al. 2014

Basic Clin Pharma Tox

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Diabetes mellitus (DM) is a major problem all over the world, affecting more people in recent years. Individuals with diabetes are more prone to disease than non-diabetics, especially vascular complications. The aim of this study was to examine the roles of the endothelin (ET)-1 in brain damage formed in a streptozocin (STZ)-induced diabetes model, and the effect of bosentan, which is the non-specific ET1 receptor blocker in the prevention of the diabetes-induced brain damage. To examine the effects of bosentan (50 mg/kg and 100 mg/kg) in this study, the rats were given the drug for 3 months. The rats were divided into four groups: the sham group (n = 10), the diabetic control group (n = 10), the group of diabetic rats given bosentan 50 mg/ kg (n = 10) and the group of diabetic rats given bosentan 100 mg/kg (n = 10). Diabetes was induced in the rats by STZ (60 mg/kg i.p.). On day 91, all rats were killed. Brain tissues of the rats were measured by molecular, biochemical and histopathological methods. Antioxidant levels in the therapy groups were observed as quite near to the values in the healthy group. In this study, while the brain eNOS levels in the diabetic groups decreased, the ET1 and iNOS levels were found to be increased. However, in the diabetes group, hippocampus and cerebellum, pericellular oedema and a number of neuronal cytoretraction were increased in neuropiles, whereas these results were decreased in the therapy group. Based on all of these results, ET1 will not be ignored in diabetes-induced cerebral complications.Diabetes mellitus (DM) is a severe disease which eventually results in death. During diabetes mellitus, tissues cannot uptake glucose and very severe complications such as nephropathy, retinopathy, neuropathy and peripheral vascular complications occur [1]. Many new mechanisms have been suggested during the formation and progress of these complications. There are studies in many areas, from inflammation to cellular membrane disorders, of the mechanisms of diabetesinduced complications [1][2][3]. There are also many studies on the receptors which are responsible for the formation of diabetes and diabetes-induced complications in relation to our topic: angiotensin receptors, urotensin receptors, glucagon-like peptide 1 receptors and peroxisome proliferator-activated receptora [4,5].Previous studies have shown the importance of angiotensin in diabetes-induced liver damage [6,7], and there are many recent studies showing that endothelin-1 receptors play important roles in diabetes. One study showed that cell proliferation and, at the same time, ET1 production increased in type 2 diabetes [8,9]. Diabetes-related, clinical and experimental studies showed that ET1 plasma levels increased [10,11]. A study by Mastumoto et al. showed that the expression of both ET1 and the receptors increased in the streptozotocin (STZ)-induced diabetes model [12]. In another study, giving endothelin-1 to individuals with insulin resistance reduced endothelin-1-induced vasodilatation [13]. ET1 levels w...

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“…It affects all classes of macromolecules (sugar, lipid, protein and DNA), leading inevitably to neuronal dysfunction (Moreira et al, 2005). Baydas et al (2005) has reported that STZ causes glial and neuronal cell death in animal models for diabetes.…”

Section: Discussionmentioning

confidence: 99%

Prevention of cognitive impairments and neurodegeneration by Khamira Abresham Hakim Arshad Wala

Khan

Hoda

Yousuf

et al. 2006

Journal of Ethnopharmacology

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Novel role for gabapentin in neuroprotection of central nervous system in streptozotocine-induced diabetic rats1

Cited by 51 publications

References 32 publications

Beneficial Effects ofTeucrium poliumand Metformin on Diabetes-Induced Memory Impairments and Brain Tissue Oxidative Damage in Rats

Beneficial Effects ofTeucrium poliumand Metformin on Diabetes-Induced Memory Impairments and Brain Tissue Oxidative Damage in Rats

Does Bosentan Protect Diabetic Brain Alterations in Rats? The Role of Endothelin‐1 in the Diabetic Brain

Prevention of cognitive impairments and neurodegeneration by Khamira Abresham Hakim Arshad Wala

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