Heme Oxygenase‐1 Mediated Memorial and Revivable Protective Effect of Ischemic Preconditioning on Brain Injury
| Autor: | Mei Jiang, Jing Quan, Jian Sun, Xue-Yi Li, Qiu-Jun Liang, Sifeng Chen, Xinhong Wang, Li-Li Le, Ning Li, Meng Xiang, Dan Meng |
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| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: |
Brain Infarction
Male Ischemia Protoporphyrins Pharmacology Functional Laterality chemistry.chemical_compound Physiology (medical) parasitic diseases medicine Animals Pharmacology (medical) cardiovascular diseases Enzyme Inhibitors Rats Wistar Ischemic Preconditioning Stroke Memory Disorders business.industry Receptors Purinergic P1 Original Articles medicine.disease Adenosine receptor Rats Heme oxygenase Psychiatry and Mental health chemistry Gene Expression Regulation Anesthesia Brain Injuries Ischemic preconditioning Immunohistochemistry Nervous System Diseases business Intracellular Heme Oxygenase-1 Hemin |
| Popis: | Summary Aims Ischemic preconditioning (IPC) has short-term benefits for stroke patients. However, if IPC protective effect is memorial and the role of the intracellular protective protein heme oxygenase-1 (HO-1) is not known. Methods Ischemic preconditioning and the corresponding sham control were achieved by blocking the blood flow of the left internal carotid artery for 20 min and 2 second, respectively, in rats. Both IPC and sham-operated animals were divided into three groups and treated with PBS, the HO-1 inducer hemin, and the HO-1 inhibitor Znpp. Three weeks after IPC, brain ischemia–reperfusion injury was achieved by left middle cerebral artery obstruction for 45 min followed by 24-h reperfusion. Results 2,3,5-triphenyltetrazolium chloride staining and neurological dysfunction scoring showed IPC significantly reduced brain infarct area and improved neurological function occurred 3 weeks after IPC. Hemin treatment promoted whereas ZnPP blocked the benefits of IPC. Immunohistochemical analysis and Western blotting showed that the expression of HO-1 was higher in the border zone than in the necrotic core zone. The memorial IPC protection is independent of adenosine receptor A1R and A2aR expressions. Conclusions We found for the first time that the protective effect of IPC can be remembered to protect brain injury occurred after acute response disappear. The results indicate that interventional treatment can achieve protective effect for future cerebral injury not only through interventional treatment itself but also through the memorial and revivable IPC, eliminating the concern that temporary ischemia caused by interventional treatment may leave harmful effect in the brain. |
| Databáze: | OpenAIRE |
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