Investigation of the inflammasomes' effects on the innate inflammatory response during brain ischemia

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K20342
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Emergency medicine
• Research Institution: Ehime University
• Principal Investigator: zhu pengxiang 愛媛大学, 医学系研究科, 助教 (40380216)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: インフラマソーム / 軽度外傷性脳損傷（MTBI) / 高次脳機能障害 / IL-1β / TNFα

Outline of Final Research Achievements

Inflammasomes can be activated not only by extracorporeal pathogens like virus and bacterium, but also by the internal factors including intracellular matrix to induce inflammation during neurodegeneration. ASC (apoptosis-associated speck-like protein containing a CARD) is a key component to activate inflammasomes. We investigated the effects of knock out of ASC on the severity of ischemic brain damage and traumatic brain injury. Compared to wild type, targeted disruption of ASC significantly suppressed increases in TNFα and IL-1β within the ischemic brain, and showed a tendency of less infarct volume after ischemia. Furthermore, this disruption significantly precluded increases in TNFα and IL-1β within the brain subjected to mild traumatic injury and attenuated space-navigation disability after mild traumatic brain injury (MTBI). These findings suggest that the inhibition of inflammasomes’ activation can ameliorate the secondary neurodegeneration after brain ischemia or MTBI.

Free Research Field

救急医療、脳外科。