4-Methylguaiacol alleviated alcoholic liver injury by increasing antioxidant capacity and enhancing autophagy through the Nrf2-Keap1 pathway

Li, Anjun; Chen, Shanbin; Luan, Chunguang; Lü, Wei; Hao, Feike; Tang, Youhong; Xinglin, Han; Wang, DeLiang

doi:10.1016/j.fbio.2022.102160

Cited by 3 publications

(1 citation statement)

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“…Normally, the Nrf2 is locked by Kelch-like ECH-associated protein-1 (Keap1) and Cullin3 (Cul3) with no activity in the cytoplasm [ 53 ]. After the stimulation of ROS, or oxidative stress productions, the Nrf2 will be released from the complex of Nrf2-Keap1-Culs and will transfer into the nucleus to bind with the antioxidant response element (ARE), eventually promoting the transcription of various antioxidant enzymes (GSH-Px, CAT, SOD and HO-1), GSH synthesis, and metabolism [ 54 ]. These antioxidant enzymes play vital roles in scavenging excessive ROS.…”

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%