Hyperglycemia enhances excessive superoxide anion radical generation, oxidative stress, early inflammation, and endothelial injury in forebrain ischemia/reperfusion rats

Tsuruta, Ryosuke; Fujita, Motoki; Ono, Takeru; Koda, Yoichi; Koga, Yasutaka; Yamamoto, Takahiro; Nanba, Masayuki; Shitara, Masaki; Kasaoka, Shunji; Maruyama, Ikuro; Yuasa, Makoto; Maekawa, Taira

doi:10.1016/j.brainres.2009.10.065

Cited by 69 publications

(52 citation statements)

References 34 publications

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“…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%

“…A large amount of ROS locally generated by cerebral ischemia/reperfusion induces free radical chain reactions (Saito et al, 2005), which may be enhanced by increased oxidative stress in the diabetic state. Evidence is being accumulated that oxidative stress is enhanced by hyperglycemia in the diabetic state (Kusaka et al, 2004;Rizk et al, 2005;Tsuruta et al, 2010). In the diabetic state, "glucose toxicity" caused by augmentation of intracellular glucose oxidation process and nonenzymatic glycation of protein molecules leads to over production of ROS and damage of neurons and endothelial cells (Baynes 1991).…”

Section: Discussionmentioning

confidence: 99%

“…In the diabetic state, "glucose toxicity" caused by augmentation of intracellular glucose oxidation process and nonenzymatic glycation of protein molecules leads to over production of ROS and damage of neurons and endothelial cells (Baynes 1991). Previous studies have demonstrated that the hyperglycemic condition in cerebral ischemia without diabetes exacerbates brain injury due to enhanced production of ROS in the brain (Anabela et al, 2006;Tsuruta et al, 2010). Augmented oxidative stress involving increased ROS generation, augmented lipid peroxidation and reduction of antioxidants has been indicated in the brain, kidney, pancreas and liver of STZ-induced diabetic rats (Muralikrishna Adibhatla et al, 2006).…”

Section: Discussionmentioning

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

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

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

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“…[29][30][31][32] Evidence suggests factors such as acute hyperglycemia might limit collateral status by actively promoting the constriction of leptomeningeal arteries. 33,34 Constriction could arise from the inhibitory effect of elevated glucose on voltagegated K þ channel conductance in vascular smooth muscle 34,35 or owing to the production of endothelial-derived relaxing factors like nitric oxide. 34,36 Our study, along with other previous studies, points toward large variability in the size of pial arteries in the ischemic vascular bed.…”

Section: Discussionmentioning

confidence: 99%

Assessment of Leptomeningeal Collaterals Using Dynamic CT Angiography in Patients with Acute Ischemic Stroke

Menon

O’Brien

Bivard

et al. 2012

J Cereb Blood Flow Metab

154

120

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Whole-brain dynamic time-resolved computed tomography angiography (CTA) is a technique developed on the new 320-detector row CT scanner capable of generating time-resolved cerebral angiograms from skull base to vertex. Unlike a conventional cerebral angiogram, this technique visualizes pial arterial filling in all vascular territories, thereby providing additional hemodynamic information. Ours was a retrospective study of consecutive patients with ischemic stroke and M1 middle cerebral artery þ / À intracranial internal carotid artery occlusions presenting to our center from June 2010 and undergoing dynamic timeresolved CTA and perfusion CT within 6 hours of symptom onset. Leptomeningeal collateral status was assessed by determining relative prominence of pial arteries in the ischemic region, rate and extent of retrograde flow, and various topographical patterns of pial arterial filling. Twenty-five patients were included in the study. We demonstrate the existence of the following novel properties of leptomeningeal collaterals in humans: (a) posterior (posterior cerebral artery (PCA)-MCA) dominant collateralization, (b) intraterritorial 'within MCA region' leptomeningeal collaterals, and (c) significant variability in size, extent, and retrograde filling time in pial arteries. We also describe a simple and reliable collateral grading template that, for the first time on dynamic CTA, incorporates back-filling time as well as size and extent of collateral filling.

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“…Initially, hyperglycemia induces various molecular reactions resulting in production of AGE and radical oxygen species [18,19]. AGE can bind to their receptors called RAGE, which results in the release of pro-inflammatory stimuli, including HMGB1.…”

Section: Discussionmentioning

confidence: 99%

HMGB1 suppression confers neuroprotection against stroke in diabetic rats

Kim

Choi

Jang

et al. 2013

Translational Neuroscience

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Objectives: Diabetes is a principal risk factor for stroke, and results in poorer neurological outcome after stroke. High mobility group box-1 (HMGB1) was recently reported to mediate an increased inflammatory response through receptors for advanced glycation end products (RAGE) and Toll-like receptors (TLR). In this study, we investigated how blocking HMGB1, using glycyrrhizin, may reduce inflammation following ischemic stroke in a diabetic model. Methods: The effect of glycyrrhizin on non-stroke diabetic rats was assessed, following diabetes induction by streptozotocin. This was followed with the analysis of glucose, HMGB1 and cytokines levels. We then sought to determine the impact of HMGB1 suppression with glycyrrhizin after a stroke using transient occlusion of the middle cerebral artery. Infarct volume, HMGB1 levels, expression of TLR and RAGE and their subcellular pathways were measured. Results: In the non-stroke state, glycyrrhizin did not reduce glucose levels in diabetic rats, but significantly reduced HMGB1 and interleukin (IL)-1β levels. Furthermore, glycyrrhizin decreased the infarct volume after focal cerebral ischemia in diabetic rats (140±79 mm 3 versus 224±68 mm 3 ; p=0.03). HMGB1 secretion from the ischemic brain and expression of TLR2, TLR4 and RAGE were reduced after glycyrrhizin treatment. Intracellular signaling pathways related to HMGB1 receptors, such as NF-κB, ERK, and Akt, were reduced after HMGB1 inhibition using glycyrrhizin. Discussion: Our results indicate that HMGB1 suppression by glycyrrhizin reduces the inflammatory response in diabetes with or without stroke. We conclude that HMGB1 may be a good candidate to target for the inhibition of the inflammatory response after stroke.

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Hyperglycemia enhances excessive superoxide anion radical generation, oxidative stress, early inflammation, and endothelial injury in forebrain ischemia/reperfusion rats

Cited by 69 publications

References 34 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

Assessment of Leptomeningeal Collaterals Using Dynamic CT Angiography in Patients with Acute Ischemic Stroke

HMGB1 suppression confers neuroprotection against stroke in diabetic rats

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