期刊
BIOMEDICAL REPORTS
卷 5, 期 1, 页码 11-17出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/br.2016.677
关键词
neurological impairment; inflammatory response; microglia; astrocyte; cardiac arrest; cardiopulmonary resuscitation
资金
- National Natural Science Foundation of China [81503061, 81570401, 81170136, 81300103, 81571934]
- Taishan Scholar Program of Shandong Province [ts20130911]
- Specialized Research Fund for the Doctoral Program of Higher Education [20130131110048]
- Key Technology Research and Development Program of Science and Technology of Shandong Province [2014kjhm0102]
- Department of Science and Technology of Shandong Province [2014GGE27492]
- Fundamental Research Funds of Shandong University [2014QLKY04]
Cardiac arrest (CA) is a leading cause of fatality and long-term disability worldwide. Recent advances in cardiopulmonary resuscitation (CPR) have improved survival rates; however, the survivors are prone to severe neurological injury subsequent to successful CPR following CA. Effective therapeutic options to protect the brain from CA remain limited, due to the complexities of the injury cascades caused by global cerebral ischemia/reperfusion (I/R). Although the precise mechanisms of neurological impairment following CA-initiated I/R injury require further clarification, evidence supports that one of the key cellular pathways of cerebral injury is inflammation. The inflammatory response is orchestrated by activated glial cells in response to I/R injury. Increased release of danger-associated molecular pattern molecules and cellular dysfunction in activated microglia and astrocytes contribute to ischemia-induced cytotoxic and pro-inflammatory cytokines generation, and ultimately to delayed death of neurons. Furthermore, cytokines and adhesion molecules generated within activated microglia, as well as astrocytes, are involved in the innate immune response; modulate influx of peripheral immune and inflammatory cells into the brain, resulting in neurological injury. The present review discusses the molecular aspects of immune and inflammatory mechanisms in global cerebral I/R injury following CA and CPR, and the potential therapeutic strategies that target neuroinflammation and the innate immune system.
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