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| TAK-242 confers neuroprotection in rats after cardiopulmonary resuscitation |
| Chen Ning |
| Xiuying Emergency Department, Hainan general Hospital, Haikou 570311, China |
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Abstract Objective To determine the role of TAK-242 on brain injury and neurological out⁃ come after cardiopulmonary resuscitation（CPR）in rats. Methods A total of 173 male Sprague-Daw⁃ ley rats were randomly divided into sham group（n＝20）, CPR group（n＝56）, low- dose TAK- 242 treatment group（n＝50）and high-dose TAK-242 treatment group（n＝47）. The animal model of cardiac arrest induced by asphyxia and CPR was established. TUNEL assay was used to determine apoptosis in the cerebral cortex 24 h after recovery of spontaneous circulation. Western blot was used to examine the expression of NF-κB p65 and cleaved caspase-3. Furthermore, a separate set of animals were used to determine the neurologic deficit scales（NDS）at 24, 48 and 72 h post-return of spontaneous circulation. ELISA was used to determine the expression of TNF-α, IL-1β and IL-6 in human cerebrospinal fluid and brain tissues. Results Compared with the sham operation group,the expression levels of cleaved caspase-3 and NF-κB p65, TNF-α, IL-1β and IL-6 in model group were significantly increased, and TAK-242 can significantly decrease expression levels of cleaved caspase-3，NF-κB p65, IL-6, TNF-α, IL-1β, increases the expression of NF-κB p65, while significantly reduces the number of neurons apop⁃ tosis, and it was dose dependent. Conclusion TAK-242 attenuated brain injury and improved neuro⁃ logical outcome after cardiac arrest in rats.
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Received: 04 December 2015
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| About author:: Chen Ning, E-mail: chenn4203@163.com |
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