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Published on: January 5, 2018
An effective combination of two different methods of postconditioning
Viera Danielisova1, Jozef Burda, Miroslava Nemethova
1Institute of Neurobiology, Slovak Academy of Sciences, Soltesovej 4, 040 01 Kosice, Slovakia. danielis@saske.sk
Repeated stress can induce ischemic tolerance, with protective proteins activated by subsequent stress. Combining rapid and delayed postconditioning effectively reduces neuronal damage and exploits a two-day therapeutic window for delayed neuronal death.
Area of Science:
- Neuroscience
- Cellular Biology
- Biochemistry
Background:
- Ischemic tolerance, mediated by protective proteins, strengthens with repeated stress exposure.
- Preconditioning and postconditioning are strategies involving stress application before or after ischemia.
- Antioxidants can interfere with tolerance acquisition when combined with pre/postconditioning.
Purpose of the Study:
- To investigate the efficacy of combining rapid and delayed postconditioning strategies.
- To explore the therapeutic window for intervening in delayed neuronal death.
- To assess the effectiveness of post-conditioning interventions in reducing ischemic injury.
Main Methods:
- Rapid postconditioning: 30-s reperfusion alternating with 15-s ischemia, repeated thrice immediately after lethal ischemia.
- Delayed postconditioning: Intraperitoneal injection of Bradykinin 2 days after lethal ischemia.
- Evaluation of antioxidant effectiveness in conjunction with postconditioning.
Main Results:
- Rapid postconditioning effectively reduced post-ischemic reactive oxygen species production.
- The combination of rapid and delayed postconditioning proved effective in mitigating ischemic injury.
- A two-day therapeutic window was confirmed for treating delayed neuronal death.
Conclusions:
- Combined rapid and delayed postconditioning is a viable strategy for enhancing neuroprotection.
- Delayed neuronal death, a form of apoptosis, presents a treatable condition within a specific therapeutic window.
- Interventions targeting reactive oxygen species and utilizing bradykinin show promise in managing ischemic brain injury.
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