Transient Global Ischemia-Induced Brain Inflammatory Cascades Attenuated by Targeted Temperature Management
| Autor: | Sung Phil Chung, Ji Sun Woo, Ju Hee Kim, Jin Ho Beom, Sang Won Suh, Yoo Seok Park, Dae Ki Hong, Je Sung You |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Male high mobility box protein 1 QH301-705.5 medicine.medical_treatment Ischemia microglia Inflammation Brain damage Targeted temperature management Pharmacology Neuroprotection targeted temperature management Catalysis Article Proinflammatory cytokine Body Temperature Brain Ischemia post cardiac arrest care Inorganic Chemistry Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine Hypothermia Induced Medicine Animals Physical and Theoretical Chemistry Biology (General) Molecular Biology QD1-999 Spectroscopy Neuroinflammation Brain Diseases Microglia business.industry Organic Chemistry apoptosis General Medicine medicine.disease Computer Science Applications Rats Chemistry 030104 developmental biology medicine.anatomical_structure medicine.symptom business 030217 neurology & neurosurgery |
| Zdroj: | International Journal of Molecular Sciences Volume 22 Issue 10 International Journal of Molecular Sciences, Vol 22, Iss 5114, p 5114 (2021) |
| ISSN: | 1422-0067 |
| Popis: | Sudden cardiac arrest leads to a significantly increased risk of severe neurological impairment and higher mortality rates in survivors due to global brain tissue injury caused by prolonged whole-body ischemia and reperfusion. The brain undergoes various deleterious cascading events. Among these damaging mechanisms, neuroinflammation plays an especially crucial role in the exacerbation of brain damage. Clinical guidelines indicate that 33 °C and 36 °C are both beneficial for targeted temperature management (TTM) after cardiac arrest. To clarify the mechanistic relationship between TTM and inflammation in transient global ischemia (TGI) and determine whether 36 °C produces a neuroprotective effect comparable to 33 °C, we performed an experiment using a rat model. We found that TTM at 36 °C and at 33 °C attenuated neuronal cell death and apoptosis, with significant improvements in behavioral function that lasted for up to 72 h. TTM at 33 °C and 36 °C suppressed the propagation of inflammation including the release of high mobility group box 1 from damaged cells, the activation and polarization of the microglia, and the excessive release of activated microglia-induced inflammatory cytokines. There were equal neuroprotective effects for TTM at 36 °C and 33 °C. In addition, hypothermic complications and should be considered safe and effective after cardiac arrest. |
| Databáze: | OpenAIRE |
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