AI Article Synopsis
- Cerebral ischemia is a major cause of disability, but its mechanisms are still not fully understood, especially regarding the injury that occurs when blood flow is restored.
- This study is the first to explore the role of IL-32, a pro-inflammatory factor, in cerebral ischemia-reperfusion injury, finding that it is highly expressed in models of this condition.
- Inhibiting IL-32 and blocking the related NOD/MAPK/NF-κB pathway improved cell survival and reduced inflammation, suggesting IL-32 could be a promising target for new treatment strategies.
Article Abstract
Cerebral ischemia represents a major cause of disability, yet its precise mechanism remains unknown. In addition, ischemia-reperfusion injury which occurs during the blood recovery process increases the risk of mortality, and is not adequately addressed with current treatment. To improve therapeutic options, it is important to explore the vital substances that play a pivotal role in ischemia-reperfusion injury. This study is the first to investigate the role of IL-32, a vital pro-inflammatory factor, in models of cerebral ischemia-reperfusion injury. The results showed that IL-32 was highly expressed in both in vivo and in vitro models. The proteins of the NOD/MAPK/NF-κB pathway were also up-regulated, indicating a potential signaling pathway mechanism. Inhibition of IL-32 and blocking of the NOD/MAPK/NF-κB pathway increased cell survival, decreased the level of inflammatory factors and inflammasomes, and attenuated nitrosative stress. Taken together, the results show that inhibition of IL-32 expression ameliorates cerebral ischemia-reperfusion injury via the NOD/MAPK/NF-κB signaling pathway. The findings in this study reveal that IL-32 is a vital target of ischemia-reperfusion injury, providing a new avenue for treatment development.
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| http://dx.doi.org/10.1007/s12031-020-01557-0 | DOI Listing |
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