AFG, an important maillard reaction product in red ginseng, alleviates D-galactose-induced brain aging in mice via correcting mitochondrial dysfunction induced by ROS accumulation

Zhang, Jun-jie; Chen, Ke-cheng; Yin, Ji-ying; Zheng, Yi-nan; Chen, Ri-xin; Liu, Wei; Tang, Shan; Zhang, Jing; Zhang, Ming; Wang, Zi; Liu, Shuang; Li, Wei

doi:10.1016/j.ejphar.2023.175824

Cited by 3 publications

(1 citation statement)

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“…Therefore, without the supplementation of exogenous antioxidants, the excessive ROS may result in neurological decline or cognitive dysfunction in the brain, such as Alzheimer’s disease, neurodegenerative disease, etc. [ 40 ]. Particularly, the damage to the CA1, CA2, CA3, and DG regions in the brain will directly affect the transition of information from short-term to long-term memory.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Que Zui Tea on d-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway

Wang,

Zhao

et al. 2024

Molecules

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Que Zui tea (QT) is an important herbal tea in the diet of the ‘Yi’ people, an ethnic group in China, and it has shown significant antioxidant, anti-inflammatory, and hepatoprotective effects in vitro. This study aims to explore the protective effects of the aqueous-ethanol extract (QE) taken from QT against ᴅ-galactose (ᴅ-gal)-induced oxidative stress damage in mice and its potential mechanisms. QE was identified as UHPLC-HRMS/MS for its chemical composition and possible bioactive substances. Thus, QE is rich in phenolic and flavonoid compounds. Twelve compounds were identified, the main components of which were chlorogenic acid, quinic acid, and 6′-O-caffeoylarbutin. Histopathological and biochemical analysis revealed that QE significantly alleviated brain, liver, and kidney damage in ᴅ-gal-treated mice. Moreover, QE remarkably attenuated oxidative stress by activating the Nrf2/HO-1 pathway to increase the expression of antioxidant indexes, including GSH, GSH-Px, CAT, SOD, and T-AOC. In addition, QE administration could inhibit the IL-1β and IL-6 levels, which suppress the inflammatory response. QE could noticeably alleviate apoptosis by inhibiting the expressions of Caspase-3 and Bax proteins in the brains, livers, and kidneys of mice. The anti-apoptosis mechanism may be related to the upregulation of the SIRT1 protein and the downregulation of the p53 protein induced by QE in the brain, liver, and kidney tissues of mice. Molecular docking analysis demonstrated that the main components of QE, 6′-O-caffeoylarbutin, chlorogenic acid, quinic acid, and robustaside A, had good binding ability with Nrf2 and SIRT1 proteins. The present study indicated that QE could alleviate ᴅ-gal-induced brain, liver and kidney damage in mice by inhibiting the oxidative stress and cell apoptosis; additionally, the potential mechanism may be associated with the SIRT1/Nrf2 signaling pathway.

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Section: Discussionmentioning

confidence: 99%