Diabetes enhances apoptosis induced by cerebral ischemia

Li, Zhen Guo; Britton, Mark; Sima, Anders A. F.; Dunbar, Joseph C.

doi:10.1016/j.lfs.2004.03.039

Cited by 63 publications

(61 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, we observed that the post-ischemic induction of MPO and ICAM-1, which are hallmarks of neutrophil and macrophage/microglia activation and extravasation, was significantly increased in the diabetic rat brain indicating exaggeration of inflammatory responses in ischemic injury. Our present data are in agreement with other studies describing the exacerbated inflammation in diabetic model animals (Li et al, 2004;Tsuruta et al 2010;Tureyen et al, 2011). For example, a model of type-2 diabetes db/db mouse that has a point mutation of the leptin receptor showed increased brain damage and higher expression levels of IL-1, IL-6, ICAM-1, MPO and other inflammatory markers as compared with the db/+ control after MCAO/Re (Tureyen et al, 2011).…”

Section: Discussionsupporting

confidence: 92%

“…The percentage of apoptotic cells was calculated by the apoptotic index, i.e. dividing the number of positive-staining nuclei by the total number of nuclei (Li et al, 2004 …”

Section: Tunel Stainingmentioning

confidence: 99%

“…Additionally, they are more likely to have a poor prognosis and increased mortality after stroke (Biller et al, 1993;Vinik et al, 2002). Previous studies have demonstrated that the diabetic state increases oxidative stress in the brain and aggravates cerebral ischemic injury in both type I (Li et al, 2004;Saito et al, 2005;Rizk et al, 2005) and type II diabetic animal models (Anabela et al, 2006;Tureyen et al, 2011). In addition to neuronal damage attributed to hypoxia and ATP depletion caused by vascular obstruction in ischemic core region, cerebral injury caused by subsequent reperfusion is also involved in the pathophysiology of transient ischemia (Doyle et al, 2008;Nakka et al, 2008;Wang et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Diabetes-Mediated Exacerbation of Neuronal Damage and Inflammation After Cerebral Ischemia in Rat: Protective Effects of Water-Soluble Extract from Culture Medium of Ganoderma lucidum Mycelia

Iwata¹,

Okazaki²,

Nakano³

et al. 2012

Advances in the Preclinical Study of Ischemic Stroke

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 92%

“…The percentage of apoptotic cells was calculated by the apoptotic index, i.e. dividing the number of positive-staining nuclei by the total number of nuclei (Li et al, 2004 …”

Section: Tunel Stainingmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Diabetes-Mediated Exacerbation of Neuronal Damage and Inflammation After Cerebral Ischemia in Rat: Protective Effects of Water-Soluble Extract from Culture Medium of Ganoderma lucidum Mycelia

Iwata¹,

Okazaki²,

Nakano³

et al. 2012

Advances in the Preclinical Study of Ischemic Stroke

View full text Add to dashboard Cite

“…The cognitive impairment associated with type 1 diabetes has been linked to apoptosis-induced neuronal loss in the hippocampus (30). Moreover, diabetes not only induces apoptosis but also enhances apoptosis induced by other pathological conditions, such as cerebral ischemia (50). To our knowledge, our findings are the first of their kind to suggest that hyperglycemic conditions during development produce abnormal apoptotic stress in the neocortex.…”

Section: Discussionmentioning

confidence: 56%

Hyperglycemia Inhibits Retinoic Acid–Induced Activation of Rac1, Prevents Differentiation of Cortical Neurons, and Causes Oxidative Stress in a Rat Model of Diabetic Pregnancy

2006

View full text Add to dashboard Cite

Diabetes is a risk factor for neuronal dysfunction. Impairment in signaling mechanisms that regulate differentiation of neurons is hypothesized to be one of the main causes of neuronal dysfunction. Retinoic acid, a physiologically active retinoid synthesized from vitamin A, regulates neuronal differentiation during embryonic development and is required for maintenance of plasticity in differentiated neurons. To date, little is known about the molecular events underlying hyperglycemia-induced complications in the central nervous system (CNS). Here, we provide evidence, in a diabetes rat model, of hyperglycemia-induced oxidative stress along with apoptotic stress in developing cortical neurons isolated from 16-day-old rat embryos. We also demonstrate impaired retinoic acid signaling that is involved in neuronal differentiation. Retinoic acid-induced neurite outgrowth and expression of neuronal markers were reduced in this model. The activation of small-molecular weight G-protein, Rac1, that mediates these effects was also reduced. Retinoic acid applied at a physiological concentration significantly decreased hyperglycemia-induced oxidative stress and thus supported the antioxidant defense system. These results suggest that diabetes-induced neuronal complications during pregnancy might be due to impaired retinoic acid signaling, and exogenously administered retinoic acid may be useful against CNS complications associated with diabetes. Diabetes 55: 3326 -3334, 2006

show abstract

“…Diabetes may enhance the development of stroke via increased cortical apoptotic activity but this was not additive in the hippocampus following ischemic injury (Li et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Alterations of the Giant Pyramidal Neurons (Betz Cells) in Brain Cortex of Rat Offspring Born from Gestational Diabetic Dams: A Morphometric Study

Ghafari

Golalipour

2015

Int. J. Morphol.

View full text Add to dashboard Cite

GHAFARI, S.; GOLALIPOUR, E. & GOLALIPOUR, M. J.Alterations of the giant pyramidal neurons (Betz cells) in brain cortex of rat offspring born from gestational diabetics dams: a morphometric study. Int. J. Morphol., 33(3):1120-1125, 2015. SUMMARY:A few studies reported the adverse effects of gestational diabetes on hippocampus and spinal cord of rat offspring. Giant pyramidal neurons are giant pyramidal neurons located in fifth layers of the gray matter in the primary motor cortex. Therefore, this study was conducted to determine the effect of gestational diabetes on the giant pyramidal neurons and the thickness of internal pyramidal layer in the brain cortex of rat offspring. On day 1 of gestation, 10 Wistar rat dams were randomly allocated into two control and diabetic groups. Five animals in diabetic group received 40 mg/kg/BW of Streptozotocin (intraperitoneally) and control animals received normal saline. We randomly selected six offspring of every subject in both groups at day 28, 56 and 84. Rat offspring were scarified and then coronal sections were taken from the right brain cortex and sections were stained with Cresyl violet. The density of giant pyramidal neurons in brain cortex and thickness of internal pyramidal layer of brain cortex were evaluated. In P28, P56, P84 the Betz cells density of brain cortex were significantly reduced from 107.6±6.2, 131.6±4.6 and 143.5±4.0 in controls to 84.96±2.1, 109.8±7.3 and 121.05±5.6 in cases (p<0.05), respectively. The thickness of the internal pyramidal layer of brain cortex in P28, 56 and P84 was significantly higher in gestational diabetic group in comparison with the control group (p<0.05). This study showed that uncontrolled gestational diabetes reduces the giant pyramidal neurons density and internal pyramidal layer thickness in brain cortex of rat offspring.

show abstract

Diabetes enhances apoptosis induced by cerebral ischemia

Cited by 63 publications

References 44 publications

Diabetes-Mediated Exacerbation of Neuronal Damage and Inflammation After Cerebral Ischemia in Rat: Protective Effects of Water-Soluble Extract from Culture Medium of Ganoderma lucidum Mycelia

Diabetes-Mediated Exacerbation of Neuronal Damage and Inflammation After Cerebral Ischemia in Rat: Protective Effects of Water-Soluble Extract from Culture Medium of Ganoderma lucidum Mycelia

Hyperglycemia Inhibits Retinoic Acid–Induced Activation of Rac1, Prevents Differentiation of Cortical Neurons, and Causes Oxidative Stress in a Rat Model of Diabetic Pregnancy

Alterations of the Giant Pyramidal Neurons (Betz Cells) in Brain Cortex of Rat Offspring Born from Gestational Diabetic Dams: A Morphometric Study

Contact Info

Product

Resources

About