热应激通过ROS激活的NLRP3炎性体诱导IL-1β和IL-18过度分泌:与中暑小鼠的神经炎症有关。

IF 1.6 4区 医学 Q4 NEUROSCIENCES Neuroreport Pub Date : 2024-06-05 Epub Date: 2024-04-29 DOI:10.1097/WNR.0000000000002042
Guoqiang Du, Zixi Yang, Yin Wen, Xusheng Li, Wenhong Zhong, Zhuo Li, Shiying Zhang, Ensi Luo, Hongguang Ding, Weifeng Li
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引用次数: 0

摘要

中暑通过神经炎症诱发脑损伤。本研究旨在探讨热应激是否会通过活性氧(ROS)促进NOD样受体蛋白3(NLRP3)炎性体。小鼠被随机分为假组、热应激组和热应激+TEMPOL(ROS清除剂)组。NLRP3-/-小鼠被应用并分为NLRP3-/-+假组和NLRP3-/-+热应激组。此外,在采取干预措施后,将 BV2 细胞分为四组:热应激 + TEMPOL 组、热应激 + Z-VAD-FMK(caspase-1 抑制剂)组、热应激组和对照组。检测 ROS 水平。通过 Western 印迹和双重免疫荧光检测了 NLRP3、caspase-1、IL-1β 和 IL-18 的表达水平。我们发现,热应激攻击会诱导小胶质细胞产生过量的 ROS,进而激活小鼠和 BV2 细胞中的 NLRP3 炎性体。清除ROS后,NLRP3的表达水平被下调。此外,随着 NLRP3 炎性体的激活,caspase-1、IL-1β 和 IL-18 的表达水平也升高了。但在 NLRP3-/- 小鼠中,caspase-1、IL-1β 和 IL-18 的表达水平明显下降。进一步的实验表明,预处理 caspase-1 抑制剂可降低 IL-1β 和 IL-18 的表达水平。这些结果表明,热应激攻击通过过量的 ROS 激活小胶质细胞中的 NLRP3 炎性体引起神经炎症。
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Heat stress induces IL-1β and IL-18 overproduction via ROS-activated NLRP3 inflammasome: implication in neuroinflammation in mice with heat stroke.

Heat stroke induced cerebral damage via neuroinflammation. This study aimed to approach whether heat stress would promote NOD-like receptor protein 3 (NLRP3) inflammasome via reactive oxygen species (ROS). The mice were randomly divided into the sham group, the heat stress group, and the heat stress + TEMPOL (ROS scavenger) group. And the NLRP3 -/- mice were applied and divided into the NLRP3 -/-  + sham group and the NLRP3 -/-  + heat stress group. Furthermore, the BV2 cells were divided into four groups following the intervention measures: the heat stress + TEMPOL group, the heat stress + Z-VAD-FMK (caspase-1 inhibitor) group, the heat stress group, and the control group. ROS levels were examined. The expression levels of NLRP3, caspase-1, IL-1β, and IL-18 were detected by western blotting and double immunofluorescence. We found that heat stress attack induced excessive ROS in microglia and subsequently activated NLRP3 inflammasome in both mice and BV2 cells. When ROS scavenged, the expression level of NLRP3 was downregulated. Furthermore, with NLRP3 inflammasome activation, the expression levels of caspase-1, IL-1β, and IL-18 were increased. In NLRP3 -/- mice, however, the caspase-1, IL-1β, and IL-18 were significantly declined. Further experiments showed that pretreatment of caspase-1 inhibitor decreased the expression levels of IL-1β and IL-18. These results suggest that heat stress attack caused neuroinflammation via excessive ROS activating the NLRP3 inflammasome in microglia cells.

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来源期刊
Neuroreport
Neuroreport 医学-神经科学
CiteScore
3.20
自引率
0.00%
发文量
150
审稿时长
1 months
期刊介绍: NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool. The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works. We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.
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