Effect of Streptozotocin-Induced Diabetes and Incomplete Global Cerebral Ischemia on Apoptosis in the Rat Thymus

Author(s):  
A. V. Tkachuk
1998 ◽  
Vol 274 (4) ◽  
pp. H1293-H1300 ◽  
Author(s):  
Marguerite T. Littleton-Kearney ◽  
Patricia D. Hurn ◽  
Thomas S. Kickler ◽  
Richard J. Traystman

Platelets are implicated as etiologic agents in cerebral ischemia and as modulators of neural injury following an ischemic insult. We examined the effects of severe, transient global ischemia on platelet aggregation during 45-min ischemia and 30-, 60-, and 120-min reperfusion in adult and neonatal lambs. We also examined postischemic platelet deposition in brain and other tissues (120-min reperfusion) using indium-111-labeled platelets. Ischemic cerebral blood flow fell to 5 ± 1 and 5 ± 2 ml ⋅ min−1⋅ 100 g−1in lambs and sheep, respectively. During ischemia, platelet counts fell to 47.5 ± 5.1% of control ( P < 0.05) in lambs and 59 ± 4.9% of control in sheep ( P < 0.05). Ischemia depressed platelet aggregation response ( P < 0.01) to 4 μg collagen in lambs and sheep (20.4 ± 29.2 and 26 ± 44.7% of control, respectively). Marked platelet deposition occurred in brain and spleen in sheep, whereas significant platelet entrapment occurred only in brain in lambs. Our findings suggest that ischemia causes platelet activation and deposition in brain and noncerebral tissues.


Stroke ◽  
1997 ◽  
Vol 28 (1) ◽  
pp. 198-205 ◽  
Author(s):  
Steve Davis ◽  
Mark A. Helfaer ◽  
Richard J. Traystman ◽  
Patricia D. Hurn

2013 ◽  
Vol 47 (3) ◽  
pp. 406-410 ◽  
Author(s):  
V. V. Stavchanskii ◽  
T. V. Tvorogova ◽  
A. Yu. Botsina ◽  
S. A. Limborska ◽  
V. I. Skvortsova ◽  
...  

2016 ◽  
Vol 4 (01) ◽  
pp. 63-73 ◽  
Author(s):  
Rozina Parul ◽  
Md. Jahir Alam ◽  
Md. Sohel Rana

Background: Diabetes is recognized as one of the leading causes of morbidity and mortality and representing as an emerging global epidemic worldwide. Diabetes and stroke both are the conditions which share various common threats. A patient with Diabetes has higher risk of stroke as compared to non Diabetics. Diabetes and stroke both affects the blood vessels. There are several biochemical pathways which are responsible for the developments of vascular complications due to hyperglycemia. Thus prevention and treatment of diabetes and stroke can reduce the risk of various vascular diseases. Cinnamomum zeylanicum has been used for the treatment of diabetes since long time. Cinnamomum zeylanicum rich in phenolic contents (antioxidants) have been identified as a major active component exhibiting antioxidant, and neuroprotective effects. The present study evaluate the neuroprotective effect of Cinnamomum zeylanicum in streptozotocin induced diabetes in mice and experimentally induced global cerebral ischemia/reperfusion injury in mice. Materials and methods: Swiss albino mice (male) weighing 20-30 g were randomized into eight groups. Diabetes was induced by administering streptozotocin (65 mg/kg, i.p).Starting from seven days after streptozotocin injection, insulin and Cinnamomum zeylanicum were administered for 3 weeks. Serum glucose level and body weight were measured weekly. Neuroprotective activity was carried out by global cerebral ischemia on swiss albino mice by carotid artery occlusion for 10 min followed by 24 hr. reperfusion. Measurement of Triglycerides, Malondialdehyde , cerebral infarct size and glutathione level was carried out at the end of the study. Results: After 21 days of treatment with Cinnamomum zeylanicum (75 mg/kg, 150 mg/kg and 300 mg/kg, p.o) significant increase in body weight and glutathione level and a significant reduction in serum glucose level, triglycerides, MDA levels and cerebral infarct size was observed as compared to diabetic control and diabetic+ stroke group. Conclusion: The present study concludes that Polyphenolic fraction of Cinnamomum zeylanicum not only attenuates the diabetes but also reverse the cerebral infarction in mice through its neuroprotective actions and thus Cinnamomum zeylanicum may serves as a new therapeutic alternative for management of brain damage associated with type-1 diabetes.


1991 ◽  
Vol 23 (3) ◽  
pp. 227-232 ◽  
Author(s):  
Usha S. Vasthare ◽  
Sharon Rubin ◽  
Howard A. Riina ◽  
Robert H. Rosenwasser ◽  
Christer Carlsson ◽  
...  

Author(s):  
R.V.W. Dimlich ◽  
M.H. Biros

In severe cerebral ischemia, Purkinje cells of the cerebellum are one of the cell types most vulnerable to anoxic damage. In the partial (forebrain) global ischemic (PGI) model of the rat, Paljärvi noted at the light microscopic level that cerebellar damage is inconsistant and when present, milder than in the telencephalon, diencephalon and rostral brain stem. Cerebellar injury was observed in 3 of 4 PGI rats following 5 minutes of reperfusion but in none of the rats after 90 min of reperfusion. To evaluate a time between these two extremes (5 and 90 min), the present investigation used the PGI model to study the effects of ischemia on the ultrastructure of cerebellar Purkinje cells in rats that were sacrificed after 30 min of reperfusion. This time also was chosen because lactic acid that is thought to contribute to ischemic cell changes in PGI is at a maximum after 30 min of reperfusion.


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