Effect of streptozotocin-induced diabetes mellitus on the cerebellar cortex of adult male albino rats

Selim, Sally A.; Selim, Assmaa O.

doi:10.1097/01.ehx.0000424090.98199.b8

Cited by 12 publications

(15 citation statements)

References 38 publications

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“…Further image analysis on cell quantification revealed the presence of numerous neuronal cells in diseased ZF with some large cellular globules compared to DG treated ZF groups. This alteration in cell morphology, size and volume is in agreement with a previous study that when the brain is insulted chemically and mechanically, hypertrophy and proliferation is enhanced due to structural and functional changes (Selim and Selim, 2013). This contributes to neurotoxicity from inflammatory cytokines and free radical with subsequent neuronal damage that severely contributes to the pathogenesis of neurodegenerative disease (Baydas et al, 2006;Bates et al, 2002).…”

Section: Discussionsupporting

confidence: 92%

Protective role of diosgenin against hyperglycaemia-mediated cerebral ischemic brain injury in zebrafish model of type II diabetes mellitus

Oyelaja-Akinsipo

Dare

Katare

2020

Heliyon

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Impairment in glucose regulation is an indicatory effect capable of mediating multiple dysfunction such as cerebrovascular disorder with ischemia and brain damage inclusive. This study aims at investigating the glucoselowering and neuroprotective capability of Diosgenin (DG) towards hyperglycemia-induced cerebral injury in a developed type 2 diabetes mellitus (T2DM) Zebrafish (ZF) model. T2DM was developed in ZF with 20 mg/kg body weight (b.w) multiple-low dose (MLD) Streptozotocin (STZ) for 28 days. Different doses of 20 mg/kg b.w (DG1) and 40 mg/kg b.w (DG2) DG was intraperitoneally administered twice in 7 days for a period of 28 days after T2DM was completely developed. Weight and behavioral changes were monitored and the catalytic activity including the plasma glucose level of diseased and treated ZF was spectrometrically estimated. Histopathological studies were employed to image the brain pathological condition during disease and treatment. SPSS was used as the statistical tool for result analysis and comparison of data obtained. STZ significantly ( ### p < 0.001) induced hyperglycemia when compared to control as plasma glucose increases from 101.56 AE 4.52 mgdL À1 to 175.87 AE 6.00 mg/dL. Our results have indicated a marked reduction in glucose concentration from a mean average of 175.87 AE 6.00 mgdL À1 to 105.68 AE 4.48 mgdL À1 and 82.06 AE 7.27 mgdL À1 in DG 1 and DG 2 respectively. Catalytic activity significantly decreases (p < 0.05) from 206.42 AE 30.77 unit/mL to 123.85 AE 29.99 unit/mL at a minimum and maximum value of 103.21 and 275.23 in diseased ZF respectively. On DG treatment, catalytic activity significantly (p < 0.01) rise from 101. 58 AE 11.29 and 130.73 AE 27.52 to 130.98 AE 17.13 and 255.96 AE 30.34 with DG1 and DG2 treatment respectively. Studies on the behavioral pattern of STZ-induced anxiolytic effect on ZF confirmed changes in the number of transitions and time spent in both Novel tank test (NTT) and Dark/light test (LDT). Histopathological analysis confirmed the cerebral cortex with inflammatory brain cells in the diseased condition and an attenuation of damage posed revealed in diseased state was largely reversed with DG. As compared to the normal control, a significant ( # p < 0.05 and ### p < 0.001) changes in weight of fishes were recorded and DG1 and DG2 significantly promotes (***p < 0.001) body weight and improves the irregularities in weight of ZF during disease progression. Our study confirms that the potential of DG towards the management of hyperglycemia and hyperglycemia-mediated cerebral ischemic injury is through its blood glucose-lowering properties, anti-inflammatory activity, antioxidant effect, and anxiolytic capabilities.

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Section: Discussionsupporting

confidence: 92%

Protective role of diosgenin against hyperglycaemia-mediated cerebral ischemic brain injury in zebrafish model of type II diabetes mellitus

Oyelaja-Akinsipo

Dare

Katare

2020

Heliyon

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“…In addition, separated presynaptic vesicles in swollen axonal terminals and a significant increase in the number of glial fibrillary acid protein (GFAP) astrocytes were observed in accordance with our study and other reports. The cerebellar cortex was susceptible to hyperglycemia-induced oxidative stress, which contributed to the neuronal damage and increased astrocyte activity (8). Immunohistochemical studies that evaluated the effects of STZ-induced diabetes on the nervous system of rats with 6 weeks or longer duration of diabetes have shown significant increases in the GFAP and S-100b constituents in diabetics compared to nondiabetic controls (1).…”

Section: Discussionmentioning

confidence: 99%

Analysis of diabetes-related cerebellar changes in streptozotocin-induced diabetic rats

Özdemir¹,

Akbaş²,

Kotil³

et al. 2016

Turk J Med Sci

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IntroductionDiabetes mellitus (DM) comprises a group of common metabolic disorders that share the phenotype of hyperglycemia, leading to damage in a number of tissues. Retinas, neurons, and kidneys are especially affected (1). Acute and chronic complications may occur. Chronic complications are divided into vascular and nonvascular complications. Vascular complications are subdivided into microvascular (retinopathy, neuropathy, nephropathy) and macrovascular complications (coronary artery disease, peripheral vascular disease, cerebrovascular disease). Oxidative stress, glycosylation, and protein kinase-C activation are shown in all tissues affected by microvascular complications (1-3). Glucose homeostasis in humans is important for the functioning of the nervous system. The brain is an insulin-sensitive organ with widespread and selective expression of the insulin receptor in the olfactory bulb, hypothalamus, hippocampus, amygdala, cerebral cortex, and cerebellum; hypoglycemia and hyperglycemia affect the central and peripheral nervous system, leading to severe dysfunction (1-3).Chronic hyperglycemia is associated with functional and structural blood-brain barrier (BBB) changes in cerebral microvessels (3). Diabetes is also associated with gradually developing end-organ damage in the central nervous system, known as diabetic encephalopathy, characterized by impairment of cognitive functions and electrophysiological changes. Chronically increased intracellular glucose concentration leads to functional, structural, and neurodegenerative changes (1).Studies performing biochemical and structural analysis of the brain relevant to the ultrastructural features of diabetes are limited, and the number of cerebellar studies are even more so. This study aimed to analyze the structural and ultrastructural cerebellar changes in streptozotocin (STZ)-induced diabetic rats (2,4-6). Materials and methodsTwenty male adult Sprague Dawley rats weighing 200-220 g were obtained from the Experimental Medicine Research Institute (DETAE). Fourteen of these animals were selected as the diabetic group, and after 12 h of Background/aim: Diabetic peripheral neuropathy has been extensively studied and reported, but the number of studies that have investigated diabetes-related changes in the central nervous system are limited, with even fewer studies on the cerebellum. The aim of this experimental study was to perform a histologic analysis of the diabetes-related changes in the cerebellums of diabetic rats.Materials and methods: Twenty Sprague Dawley rats weighing between 200 and 220 g were included in the study. Diabetes was induced in 14 of these rats by a single intraperitoneal injection of 65 mg/kg streptozotocin dissolved in saline, while 6 animals constituted the control group. The induction of diabetes was confirmed by measuring the blood glucose levels in the tail blood with a glucometer. Levels equal to or above 200 mg/dL were considered diabetic. Induction of diabetes failed in 3 animals, who were then excluded from the study.Results...

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“…STZ was dissolved in saline. Each rat was administered a single intraperitoneal injection of STZ at a dose of 60 mg/kg body weight freshly dissolved in 0.1 ml saline under anesthesia [9] .…”

Section: Group II (Rats Received Stz)mentioning

confidence: 99%

“…All rats that presented with a fasting blood glucose level higher than 250 mg/dl were considered diabetic [9] .…”

Section: Group II (Rats Received Stz)mentioning

confidence: 99%

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The possible protective role of melatonin on the changes in the cerebral cortex and meninges of streptozotocin-induced diabetes in adult male albino rats (histological and immunohistochemical study)

Hashem

2018

Egyptian Journal of Histology

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Introduction: Diabetes mellitus is a serious common metabolic disease. It causes a variety of functional and structural disorders in the central nervous systems. It induces alterations in the brain glucose metabolism and increase oxidative stress. Melatonin is a potent free radical scavenger and stimulates the major antioxidant enzymes. Aim: This study was aimed to evaluate the possible protective role of melatonin on the histological changes in the cerebral cortex and meninges after induction of diabetes in a rat model. Materials and Methods: In this study, forty adult male albino rats were divided into four groups (ten rats for each): Group I control rats, group II rats received intraperitoneal injection of Streptozotocin (STZ) (60 mg/kg, single dose), group III rats received intraperitoneal injection of melatonin (10 mg/kg/d) for six weeks, group IV received same previous doses of of STZ and melatonin for six weeks. At the end of experiment, the cerebral cortex was dissected and processed for light microscopic examinations and also for glial fibrillary acidic protein (GFAP) to demonstrate the astrocytes. Morphometrical and statistical analyses were carried out. Results: Examination of cerebral cortex of group II showed separation of the pia mater, congestion in the blood vessels and hemorrhage in intermediate lamella. There were multifocal histological changes and depletion of the cellular elements. The neuropil showed vacuolation. There were multiple areas of microinfarction and pericellular halos. Cresyl Violet stained sections showed karyolysis and immunohistochemical study showed significant increase in GFAP positive astrocytes. In contrary, Examination of cerebral cortex of group IV showed apparent improvement in almost all layers. Cresyl Violet stained sections showed darkly stained Nissel's granules. Immunohistochemical study showed significant decrease in GFAP positive astrocytes. Conclusion: Melatonin can ameliorate the effect of diabetes on the cerebral cortex and meninges through its antioxidant effect.

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Effect of streptozotocin-induced diabetes mellitus on the cerebellar cortex of adult male albino rats

Cited by 12 publications

References 38 publications

Protective role of diosgenin against hyperglycaemia-mediated cerebral ischemic brain injury in zebrafish model of type II diabetes mellitus

Protective role of diosgenin against hyperglycaemia-mediated cerebral ischemic brain injury in zebrafish model of type II diabetes mellitus

Analysis of diabetes-related cerebellar changes in streptozotocin-induced diabetic rats

The possible protective role of melatonin on the changes in the cerebral cortex and meninges of streptozotocin-induced diabetes in adult male albino rats (histological and immunohistochemical study)

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