期刊
INDUSTRIAL CROPS AND PRODUCTS
卷 196, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.indcrop.2023.116499
关键词
Allium chinense; Cerebral anoxia; Intracellular reactive oxygen species; NLRP3; NF-?B; Nutritional strategy
Allium chinense G. Don, known as Ganoderma of vegetables, has been used historically to treat blood stasis syndrome and reduce brain damage caused by reduced oxygen-carrying capacity. The anti-hypoxic effect of A. chinense was investigated using a mouse model of cerebral anoxia, and 16 compounds were isolated, showing potential anoxia-tolerant activity in vitro. These compounds also regulated oxidative stress markers and suppressed the expression of inflammatory proteins. This study provides a new nutritional strategy for A. chinense against cerebral anoxia and altitude illness.
Allium chinense G. Don is a popular medicinal and aromatic plant, known as Ganoderma of vegetables in history for treating blood stasis syndrome that reduces red blood cell oxygen-carrying capacity and often causes severe brain damage. However, the effect of A. chinense on cerebral anoxia remains obscure. Here, the anti-hypoxic effect of A. chinense was investigated for the first time through the cerebral anoxia model of mice. Subsequent a bio-guided investigation brought about the isolation of 16 compounds, including 9 phenolic derivatives (2 new compounds (compound 1, 8) and one new natural product (compound 2), 4 steroidal saponins and 3 fatty acid monoglycerides, among which, 6 compounds (1-4, 7, 16) exhibited significant anoxia-tolerant activity in vitro. Moreover, the release of reactive oxygen species (ROS) was decreased significantly, and glutathione (GSH) and lactate dehydrogenase (LDH) were regulated by the 6 bioactive compounds in oxygen-glucose deprivation/ reoxygenation (OGD/R)-induced BV-2 cells damage. Besides that, protein expressions of HIF-1 alpha, NLRP3, COX-2, NF-kappa B p65 and IL-18 were suppressed effectively. The investigation provided a new nutritional strategy for A. chinense against cerebral anoxia and altitude illness, which might be partially mediated by downregulating NLRP3/NF-kappa B.
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