Hyperglycemia in diabetic rats reduces the glutathione content in the aortic tissue

Tachi, Yoichi; Okuda, Yukichi; Bannai, Chieko; Bannai, Shiro; Shinohara, Mitsuko; Shimpuku, Hitomi; Yamashita, Kamejiro; Ohura, Kiyoshi

doi:10.1016/s0024-3205(01)01183-3

Cited by 38 publications

(20 citation statements)

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“…Moreover, elevated lipid peroxidation in the STZ-induced diabetic untreated group may be due to the observed reduction in GST and GSH. This is in accordance with previous publications [26][27][28][29] . Our results showed that the STZ-induced diabetic rats were subjected to oxidative stress, as was revealed by the high NO levels and high MDA levels.…”

Section: Discussionsupporting

confidence: 94%

Effects of <i>Nigella sativa</i> Oil and Thymoquinone on Oxidative Stress and Neuropathy in Streptozotocin-Induced Diabetic Rats

2009

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We examined whether Nigella sativa (NS) oil and its active constituent thymoquinone (TQ) attenuate oxidative stress in the heart and brain in an experimental model of diabetes mellitus using streptozotocin (STZ). Oxidative stress was assessed by measuring cardiac and brain nitric oxide (NO), lipid peroxide levels, glutathione (GSH) and antioxidant enzyme activities, i.e. glutathione-S-transferase (GST) and catalase. Cardiac metabolic damage was estimated by measuring cardiac creatine kinase muscle and brain types (CK-MB). Brain monoamine levels were also evaluated. STZ diabetes induced a significant increase in heart and brain NO and malondialdehyde concentrations compared with the control group. These changes were attenuated by posttreatment of rats with NS oil and TQ. STZ diabetes induced oxidative stress via a significant decrease in GST, GSH and catalase. These lowered levels were improved by either NS oil or TQ administration. Serum CK-MB was decreased in the diabetic rats, which recovered with NS oil and TQ administration. During the course of diabetes, there was a marked increase in norepinephrine and dopamine concentrations and a marked decrease in serotonin concentration compared to the control group. These findings were partly reversed by oral administration of either NS oil or TQ. It is concluded that NS and TQ correct STZ-diabetes-induced alterations in CK-MB and brain monoamines due to their antioxidant properties.

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Section: Discussionsupporting

confidence: 94%

Effects of <i>Nigella sativa</i> Oil and Thymoquinone on Oxidative Stress and Neuropathy in Streptozotocin-Induced Diabetic Rats

2009

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“…The potential reason of the increase in lipid peroxidation in STZ induced DM group may be the decrease of GSH levels. In accordance with the previous studies (Tachi et al 2001;Dincer et al 2002), Baydas et al (Baydas et al 2003) have reported that untreated diabetes generally causes lower GSH levels in different areas of the brain. Moreover, we also represented in the present study that GSH levels in the crocin treated diabetes group were significantly higher than the untreated diabetes group.…”

Section: Discussionsupporting

confidence: 90%

Neuro-protective effects of Crocin on brain and cerebellum tissues in diabetic rats

Altinzo¹,

Oner²,

Elbe³

et al. 2015

Afr. J. Trad. Compl. Alt. Med.

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Background: Increase in free oxygen radicals and the disruption of defense system make the neurons and astrocytes more sensitive against oxidative damage. Materials and Methods: Rats were divided into three groups containing 10, rats in each group namely: control (C) group, Diabetes Mellitus (DM) group, and Diabetes Mellitus + crocin (DM+crocin) group. Tissue samples were processed by routine histological and biochemical procedures. The sections were stained with Hematoxylen-eosin. Malondialdehyde (MDA), glutathione (GSH), blood glucose, HbA1c levels and xanthine oxidase (XO) activities were assayed. Results: The histological appearence of the cerebrum and cerebellum were normal in the control group. DM group showed some histopathological changes including congestion, perivascular and perineuronal edema in cerebrum. In DM + crocin group, histopathological changes in cerebrum and cerebellum markedly reduced. MDA level and XO activities increased significantly in DM group (P<0.01), but decreased significantly in DM + crocin group when compared to DM group (P<0.01). Blood glucose concentrations increased significantly (p<0.01) in DM group), but decreased significantly in DM + crocin group when compared with DM group (p<0.05). Blood HbA1c levels were normal in control group. But there were significant differences between control and DM groups (p<0.01). On the other hand, blood HbA1c levels decreased in DM+crocin group when compared with the DM group, but it was not statistically significant (p > 0.05). Conclusion: Due to the fact that crocin has an antioxidant and anti-hyperglycemic effects, it can protect the brain and cerebellum tissue against the complications of oxidative stress.

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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: Discussionsupporting

confidence: 40%

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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Hyperglycemia in diabetic rats reduces the glutathione content in the aortic tissue

Cited by 38 publications

References 0 publications

Effects of <i>Nigella sativa</i> Oil and Thymoquinone on Oxidative Stress and Neuropathy in Streptozotocin-Induced Diabetic Rats

Effects of <i>Nigella sativa</i> Oil and Thymoquinone on Oxidative Stress and Neuropathy in Streptozotocin-Induced Diabetic Rats

Neuro-protective effects of Crocin on brain and cerebellum tissues in diabetic rats

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

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