Avenanthramide C from Oats Protects Pyroptosis through Dependent ROS-Induced Mitochondrial Damage by PI3K Ubiquitination and Phosphorylation in Pediatric Pneumonia,Journal of Agricultural and Food Chemistry

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Avenanthramide C from Oats Protects Pyroptosis through Dependent ROS-Induced Mitochondrial Damage by PI3K Ubiquitination and Phosphorylation in Pediatric Pneumonia
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2022-02-04 , DOI: 10.1021/acs.jafc.1c06223
Zhichen Pu _{1,

2} , Chaozhuang Shen ₁ , Weiwei Zhang ₃ , Haitang Xie ₁ , Wusan Wang ₄

Affiliation

Oat containing rich β-glucan, polyphenols, flavonoids, saponins, alkaloids, and other substances shows good biological activities. Therefore, the present study aimed to uncover the possible mechanism and therapeutic effect of Avenanthramide C in lessening inflammatory responses in pediatric pneumonia. Pediatric pneumonia was induced by liposaccharide (LPS) for vivo model and vitro model. Macrophage was performed to determine the mechanism and effects of Avenanthramide C in pediatric pneumonia. NLRP3 activity participated in the effects of Avenanthramide C in pediatric pneumonia. Avenanthramide C induced p-PI3K and p-Akt expressions and reduced ubiquitination of PI3K expression in pediatric pneumonia. On the other hand, Avenanthramide C integrated serine at 821 sites of the PI3K protein function. Avenanthramide C reduced ROS (reactive oxygen species)-induced mitochondrial damage by PI3K/AKT function in a model of pediatric pneumonia. Avenanthramide C protects pyroptosis in a model of pediatric pneumonia by PI3K/AKT/Nrf2/ROS signaling. Taken together, our results demonstrated that Avenanthramide C protects pyroptosis through dependent ROS-induced mitochondrial damage by PI3K ubiquitination and phosphorylation in a model of pediatric pneumonia, suggesting its potential use for the treatment of pediatric pneumonia and other inflammatory diseases.

中文翻译：

燕麦中的 Avenanthramide C 通过 PI3K 泛素化和磷酸化引起的依赖 ROS 诱导的线粒体损伤保护小儿肺炎中的细胞焦亡

燕麦含有丰富的β-葡聚糖、多酚、黄酮、皂苷、生物碱等物质，显示出良好的生物活性。因此，本研究旨在揭示 Avenanthramide C 减轻小儿肺炎炎症反应的可能机制和治疗效果。体内模型和体外模型采用脂糖（LPS）诱导小儿肺炎。进行巨噬细胞以确定 Avenanthramide C 在小儿肺炎中的机制和作用。NLRP3 活性参与了 Avenanthramide C 在小儿肺炎中的作用。Avenanthramide C 在小儿肺炎中诱导 p-PI3K 和 p-Akt 表达并降低 PI3K 表达的泛素化。另一方面，Avenanthramide C 在 PI3K 蛋白功能的 821 个位点整合丝氨酸。Avenanthramide C 在小儿肺炎模型中通过 PI3K/AKT 功能减少 ROS（活性氧）诱导的线粒体损伤。Avenanthramide C 通过 PI3K/AKT/Nrf2/ROS 信号传导保护小儿肺炎模型中的细胞焦亡。总之，我们的研究结果表明，在小儿肺炎模型中，燕麦酰胺 C 通过依赖 ROS 诱导的 PI3K 泛素化和磷酸化的线粒体损伤来保护细胞焦亡，这表明它可能用于治疗小儿肺炎和其他炎症性疾病。

更新日期：2022-02-04

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