scholarly journals Vascularization Pattern After Ischemic Stroke is Different in Control Versus Diabetic Rats

Stroke ◽  
2013 ◽  
Vol 44 (10) ◽  
pp. 2875-2882 ◽  
Author(s):  
Roshini Prakash ◽  
Weiguo Li ◽  
Zhi Qu ◽  
Maribeth A. Johnson ◽  
Susan C. Fagan ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Ischemic Stroke ◽  
Glycemic Control ◽  
Reperfusion Injury ◽  
Functional Outcome ◽  
Diabetic Rats ◽  
Vascular Density ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Sensorimotor Recovery

Background and Purpose— Pre-existing diabetes mellitus worsens brain functionality in ischemic stroke. We have previously shown that type 2 diabetic rats exhibit enhanced dysfunctional cerebral neovascularization and when these rats are subjected to cerebral ischemic reperfusion injury develop hemorrhagic transformation and greater neurological deficits. However, our knowledge of vascular and functional plasticity during the recovery phase of diabetic stroke is limited. This study tested the hypothesis that vascular repair is impaired in the poststroke period in diabetes mellitus, and this is associated with poor sensorimotor and cognitive function. We further hypothesized that glycemic control prevents impaired vascularization and improves functional outcome in diabetes mellitus. Methods— Vascularization was assessed in the ipsilateral and contralateral hemispheres in control, diabetes mellitus and diabetes mellitus plus metformin groups 14 days after ischemic reperfusion injury, as well as in respective sham controls. Three-dimensional reconstruction of the fluorescein isothiocyanate (FITC)-stained vasculature was achieved by confocal microscopy, and stereological parameters, including vascular volume and surface area, were measured. Astrogliosis was determined by glial fibrillary acidic protein staining. The relative rates of sensorimotor recovery, cognitive decline, and spontaneous activity were assessed. Results— Vascular density in the peri-infarct area was significantly reduced in diabetes mellitus, whereas there was reparative neovascularization in control rats. Astroglial swelling and reactivity were more pronounced in diabetic stroke compared with control stroke. Diabetes mellitus blunted sensorimotor recovery and also exacerbated anxiety-like symptoms and cognitive deficits. Glycemic control started after stroke partially prevented these changes. Conclusions— Diabetes mellitus impairs poststroke reparative neovascularization and impedes the recovery. Glycemic control after stroke can improve neurovascular repair and improve functional outcome.

Abstract 90: Diabetes Impairs Post-stroke Cerebrovascular Plasticity And Long-term Functional Recovery.

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Roshini Prakash ◽  
Weiguo Li ◽  
Zhi Qu ◽  
Susan C Fagan ◽  
Adviye Ergul
Keyword(s):  
Cognitive Decline ◽  
Reperfusion Injury ◽  
Functional Recovery ◽  
Diabetic Rats ◽  
Neurological Deficits ◽  
Ischemic Reperfusion Injury ◽  
Post Stroke ◽  
Ischemic Reperfusion ◽  
Sensorimotor Recovery ◽  
The Impact

Background: Stroke associated with pre-existing diabetes worsens ischemic injury and impairs recovery. We have previously shown that type-2-diabetic rats subjected to cerebral ischemic reperfusion injury develop hemorrhagic transformation (HT) and greater neurological deficits. These diabetic rats also exhibit enhanced dysfunctional cerebral neovascularization that increases the risk of bleeding post-stroke. However, our knowledge of vascular and functional plasticity during the recovery phase of diabetic stroke is limited. This study tested the hypothesis that post-stroke neovascularization is impaired in diabetes and this is associated with poor sensorimotor and cognitive outcomes. Methods: Reparative neovascularization was assessed in the lesional and non-lesional areas in diabetic rats after 14 days of ischemic reperfusion injury. 3-dimensional reconstruction of the FITC stained vasculature were obtained by confocal microscopy and stereological parameters including vascular volume and surface area were measured. Astrogliosis was also determined by GFAP staining. The relative rates of sensorimotor recovery, cognitive decline and spontaneous activity were assessed. Results: Diabetes impairs reparative neovascularization in the lesional areas compared to control rats. Astroglial swelling and reactivity was pronounced in diabetic stroke compared to control stroke. Rate of sensorimotor recovery was significantly slower in diabetic stroke compared to the controls. Diabetes also exacerbated anxiety-like symptoms and cognitive decline post-stroke relative to control. Conclusion: Diabetes impairs post-stroke reparative neovascularization and impedes functional recovery. The impact of glycemic control on poor recovery in this critical period needs to be tested. N=6-8 * p≤ 0.05, ** p≤ 0.005

scholarly journals Cardiac ischemic/reperfusion injury in diabetic rats treated with a superoxide dismutase mimetic

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Dean D Schwartz ◽  
Melissa Carson ◽  
Colin B Rogers ◽  
Robert L Judd ◽  
Eric P Plaisance
Keyword(s):  
Superoxide Dismutase ◽  
Reperfusion Injury ◽  
Diabetic Rats ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion

Diabetes mellitus abrogates erythropoietin-induced cardioprotection against ischemic-reperfusion injury by alteration of the RISK/GSK-3β signaling

2010 ◽  
Vol 106 (1) ◽  
pp. 147-162 ◽  
Author(s):  
Nehmat Ghaboura ◽  
Sophie Tamareille ◽  
Pierre-Henri Ducluzeau ◽  
Linda Grimaud ◽  
Laurent Loufrani ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Reperfusion Injury ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Gsk 3Β

scholarly journals Hsp47 Inhibitor Col003 Attenuates Collagen-Induced Platelet Activation and Cerebral Ischemic–Reperfusion Injury in Rats

2022 ◽  
Vol 12 ◽  
Author(s):  
Shuang Wu ◽  
Chengwei Liang ◽  
Xiaoyun Xie ◽  
Haiping Huang ◽  
Jinfeng Fu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Protective Effect ◽  
Reperfusion Injury ◽  
Bleeding Time ◽  
Mapk Signaling ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion ◽  
Rat Platelets

Ischemic stroke is a major type of stroke worldwide currently without effective treatment, although antiplatelet therapy is an existing option for it. In previous studies, heat shock protein 47 (Hsp47) was found to be expressed on the surface of human and mice platelets and to strengthen the interaction between platelets and collagen. In recent years, Col003 was discovered to inhibit the interaction of Hsp47 with collagen. We evaluated whether the Hsp47 inhibitor Col003 is a promising therapeutic agent for ischemic stroke. Here, we first verified that Hsp47 is also expressed on the surface of rat platelets, and its inhibitor Col003 significantly inhibited thrombus formation in the FeCl3-induced rat carotid arterial thrombus model. Both Col003 and clopidogrel did not alter the bleeding time or coagulation parameters, while aspirin increased the tail-bleeding time (p < 0.05). The low cytotoxicity level of Col003 to rat platelets and human liver cells was similar to those of aspirin and clopidogrel. Col003 inhibited collagen-induced platelet aggregation, adhesion, [Ca2+]i mobilization, P-selectin expression, reactive oxygen species production and the downstream signal pathway of collagen receptors. The results of the middle cerebral artery occlusion model indicated that Col003 has a protective effect against cerebral ischemic–reperfusion injury in rats. The Hsp47 inhibitor Col003 exerted antiplatelet effect and protective effect against brain damage induced by ischemic stroke through the inhibition of glycoprotein VI (GPVI)and mitogen-activated protein kinase (MAPK) signaling events, which might yield a new antiplatelet agent and strategy to treat ischemic stroke.

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