Riboflavin, vitamin B2, attenuates NLRP3, NLRC4, AIM2, and non-canonical inflammasomes by the inhibition of caspase-1 activity.
Riboflavin, vitamin B2, attenuates NLRP3, NLRC4, AIM2, and non-canonical inflammasomes by the inhibition of caspase-1 activity.
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DOI：
10.1038/s41598-020-76251-7
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发表时间：
2020-11-05
影响因子：
4.6
通讯作者：
Lee GS
中科院分区：
文献类型：
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作者：
Ahn H;Lee GS
核黄素通常作为一种营养补充剂，它在碳水化合物、脂肪和蛋白质产生能量的过程中转化为辅酶。虽然核黄素因其抗氧化特性而被认为是一种抗炎维生素，但核黄素对炎性小体的影响尚未报道。炎性小体是一种胞质监视蛋白复合物，可导致半胱天冬酶-1活化、细胞因子成熟和细胞凋亡。在本研究中，核黄素减弱了巨噬细胞中NLRP 3炎性小体活化的指标，如白细胞介素（IL）-1β、IL-18和半胱天冬酶-1的成熟和分泌; Asc焦蛋白小体的形成;以及gasdermin D的裂解。此外，在小鼠模型中，口服和腹膜给予核黄素抑制了IL-1β和IL-18的腹膜产生。从机制上讲，核黄素可以防止线粒体扰动，例如线粒体活性氧产生和线粒体DNA释放，从而触发NLRP 3炎性体组装。进一步证实核黄素破坏caspase-1的活性，并且它还抑制AIM 2、NLRC 4和非典型炎性小体。因此，核黄素具有抗氧化作用和调节炎症反应的抗炎体特性。
Riboflavin is commonly taken as a nutritional supplement, and it converts to coenzymes during the process of energy production from carbohydrates, fats, and proteins. Although riboflavin is considered to be an anti-inflammatory vitamin because of its antioxidant properties, the effects of riboflavin on inflammasome have been not reported. Inflammasome, a cytosolic surveillance protein complex, leads to the activation of caspase-1, cytokine maturation, and pyroptosis. In the present study, riboflavin attenuated the indicators of NLRP3 inflammasome activation in macrophages, such as the maturation and secretion of interleukin (IL)-1β, IL-18, and caspase-1; the formation of Asc pyroptosome; and the cleavage of gasdermin D. In addition, the oral and peritoneal administration of riboflavin inhibited the peritoneal production of IL-1β and IL-18 in a mouse model. Mechanistically, riboflavin prevented mitochondrial perturbations, such as mitochondrial ROS production and mitochondrial DNA release, which trigger the NLRP3 inflammasome assembly. Riboflavin was further confirmed to disrupt the activity of caspase-1, and it also inhibited the AIM2, NLRC4, and non-canonical inflammasomes. Therefore, riboflavin has both an antioxidant effect and an anti-inflammasome property that regulates the inflammatory response.
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影响因子：
2.2
作者：
Ahn, Huijeong;Kim, Jeongeun;Lee, Geun-Shik
通讯作者：
Lee, Geun-Shik
影响因子：
3.8
作者：
Kim, Jeongeun;Ahn, Huijeong;Lee, Geun-Shik
通讯作者：
Lee, Geun-Shik
影响因子：
30.5
作者：
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影响因子：
8.7
作者：
Man SM;Kanneganti TD
通讯作者：
Kanneganti TD
影响因子：
30.5
作者：
通讯作者：
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