2018
DOI: 10.1016/j.fct.2018.06.018
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Acteoside protects against 6-OHDA-induced dopaminergic neuron damage via Nrf2-ARE signaling pathway

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Cited by 76 publications
(30 citation statements)
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“…The results demonstrated that the bioavailability of formononetin and calycosin was reduced, the duration of formononetin was prolonged, and the absorption rate of calycosin increased. Acteoside is a primary active substance in the SNH extract and shows antioxidant and neuroprotective effects (Li, Zhou, Xu, Song, & Lu, 2018). In this study, acteoside could not be absorbed by rats in the SNH group, whereas its concentration increased in rat plasma of the QSKL group ( C max was 18.34 ng·mL −1 , AUC 0–48h was 34.93 ng/mL·h, and AUC 0–∞ was 38.10 ng/mL·h), indicating that the bioavailability was significantly enhanced after the herbal combination.…”
Section: Resultsmentioning
confidence: 99%
“…The results demonstrated that the bioavailability of formononetin and calycosin was reduced, the duration of formononetin was prolonged, and the absorption rate of calycosin increased. Acteoside is a primary active substance in the SNH extract and shows antioxidant and neuroprotective effects (Li, Zhou, Xu, Song, & Lu, 2018). In this study, acteoside could not be absorbed by rats in the SNH group, whereas its concentration increased in rat plasma of the QSKL group ( C max was 18.34 ng·mL −1 , AUC 0–48h was 34.93 ng/mL·h, and AUC 0–∞ was 38.10 ng/mL·h), indicating that the bioavailability was significantly enhanced after the herbal combination.…”
Section: Resultsmentioning
confidence: 99%
“…Thus, complex plant extracts containing multi-target agents that interact with their receptors in a pleiotropic fashion generate a pharmacological synergism that affects numerous processes, including the movement of polar metabolites across cell membranes. In this context, Li et al [26] employed a zebrafish model to demonstrate that acteoside could penetrate the blood-brain barrier, and proposed that the phenylethanoid glycoside may have a potential therapeutic effect in Parkinson's disease.…”
Section: Resultsmentioning
confidence: 99%
“…Under homeostatic conditions, Nrf2 influences mitochondrial membrane potential, fatty acid oxidation, the availability of substrates for respiration, as well as ATP synthesis [44]. But under stress conditions, Nrf2 detaches from Keap1 and translocates to the nucleus, and counteracts the promotion of ROS production through transcriptional increase of antioxidant proteins, including SOD, CAT, HO1, NQO1, GCLM and GCLC, which subsequently modulate oxidative stress, apoptosis and inflammation in diverse neurological disorders [45,46]. Previous studies have documented that after SCI, oxidative stress markers specific to lipid and protein oxidation, namely 4-HNE and 3-NT, all up-regulate in the injured tissue homogenates [47,48].…”
Section: Discussionmentioning
confidence: 99%