Cinnamon essential oil based on NLRP3 inflammasome and renal uric acid transporters for hyperuricemia

被引:12
|
作者
Wang, Xuan [1 ]
Zhou, Peijie [1 ]
Shi, Huanxian [1 ]
Wang, Wenfei [1 ]
Li, Taotao [1 ]
Tang, Tiantian [1 ]
Duan, Jiawei [1 ]
Li, Jinkai [1 ]
Xia, Ning [1 ]
Wang, Jie [1 ]
Chen, Chao [1 ]
Wang, Jinhui [1 ]
Zou, Junbo [1 ]
Shi, Yajun [1 ]
Guo, Dongyan [1 ]
Wu, Zhenfeng [2 ]
Yang, Ming [2 ]
Zhang, Xiaofei [1 ]
Sun, Jing [1 ]
机构
[1] Shaanxi Univ Chinese Med, Key Lab Basic & New Drug Res Tradit Chinese Med, Xianyang 712046, Shaanxi, Peoples R China
[2] Jiangxi Univ Tradit Chinese Med, Dept Pharmaceut, Key Lab Modern Preparat Tradit Chinese Med, Minist Educ, Nanchang 330004, Peoples R China
基金
中国国家自然科学基金;
关键词
Weighting coefficients; Metabolomics; Cinnamon essential oil; Hyperuricemia; Oxidative stress; NLRP3; inflammasome; ALLOPURINOL HYPERSENSITIVITY SYNDROME; SUSCEPTIBILITY; METABOLOMICS; ASSOCIATION; PERFORMANCE; QUALITY; GOUT;
D O I
10.1016/j.fbio.2023.103285
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Cinnamon is widely used as a medicinal herb and a culinary spice. The major bioactive component of cinnamon is cinnamon essential oil (CEO). CEO has been reported to have anti-inflammatory and antioxidant effects, but its mechanism of action is not known. In this study, metabolomics was combined with "weighting coefficients" from network pharmacology to identify key pathways and targets, differential metabolites and key metabolic pathways for the therapeutic effects of CEO on Hyperuricemia (HUA), and to precisely investigate the molecular mechanisms of the therapeutic effects of CEO on HUA. Metabolomic analysis revealed that abnormal L-glutamate metabolism and dysregulation of Arachidonic acid (AA) metabolic pathways exacerbated inflammatory responses and oxidative stress, subsequently mediating pathological changes in HUA and exacerbating renal tissue damage. Pharmacodynamic validation showed that CEO alleviated the renal inflammatory response by inhibiting hepatic xanthine oxidase activity, upregulating superoxide dismutase and glutathione peroxidase levels, and downregulating malondialdehyde levels, synergistically inhibiting NLRP3 inflammasome activation, suppressing downstream inflammatory Interleukin-1 beta (IL-1 beta) and Interleukin-18 (IL-18) secretion, and enhancing antioxidant levels. Additionally, CEO exerted renal protective effects by upregulating the renal transporters OAT1 and ABCG2 and downregulating the GLUT9 and URAT1 levels, resulting in the downregulation of uric acid production and the alleviation of renal tubular lesions. This suggests that CEO could be considered as a potential functional food for kidney damage caused by hyperuricemia.
引用
收藏
页数:17
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