Neuroprotective Effects of Peanut Skin Extract Against Oxidative Injury in HT-22 Neuronal Cells DOI Creative Commons
Jinlan Huang, Yue Zhou, Hui Xu

et al.

Pharmaceuticals, Journal Year: 2025, Volume and Issue: 18(4), P. 544 - 544

Published: April 8, 2025

Background: Oxidative stress is a key therapeutic target in neurological disorders. As processing wastes from the peanut industry, skins are great sources of antioxidants and possess potential neuroprotection. Methods: We prepared skin extract (PSE) investigated its protective effects against tert-butyl hydroperoxide (t-BHP)-induced oxidative injury HT-22 neuronal cells. Results: PSE was rich phenolic compounds (123.90 ± 0.46 mg GAE/g), comprising flavonoids (75.97 0.23 RE/g) proanthocyanidins (53.34 1.58 PE/g), displayed potent radical scavenging activities chemical-based assays. In cells, pretreatment restored balance endogenous antioxidant defense disrupted by t-BHP, as evidenced significant reductions ROS generation lipid peroxidation levels, along with enhanced antioxidants. Specifically, 25 μg/mL reduced levels 53.03%, decreased MDA content 78.82%, superoxide dismutase (SOD) activity 12.42%, improved ratio glutathione (GSH) to oxidized (GSSG) 80.34% compared t-BHP group. Furthermore, rescued mitochondrial membrane collapse, inhibited cytochrome c (Cyt.c) release, prevented subsequent apoptotic death. Notably, neuroprotective efficacy comparable that edaravone, an approved drug. Mechanistic investigations combining network pharmacology experimental validation revealed PI3K/Akt/Nrf2 signaling pathway played pivotal role mediating PSE. Compared t-BHP-treated µg/mL significantly upregulated PI3K/Akt phosphorylation, expression Nrf2, downstream proteins heme oxygenase-1 (HO-1) NAD(P)H dehydrogenase quinone 1 (NQO1). Conclusions: Collectively, these findings demonstrate natural agent oxidative-related

Language: Английский

Neuroprotective Effects of Peanut Skin Extract Against Oxidative Injury in HT-22 Neuronal Cells DOI Creative Commons
Jinlan Huang, Yue Zhou, Hui Xu

et al.

Pharmaceuticals, Journal Year: 2025, Volume and Issue: 18(4), P. 544 - 544

Published: April 8, 2025

Background: Oxidative stress is a key therapeutic target in neurological disorders. As processing wastes from the peanut industry, skins are great sources of antioxidants and possess potential neuroprotection. Methods: We prepared skin extract (PSE) investigated its protective effects against tert-butyl hydroperoxide (t-BHP)-induced oxidative injury HT-22 neuronal cells. Results: PSE was rich phenolic compounds (123.90 ± 0.46 mg GAE/g), comprising flavonoids (75.97 0.23 RE/g) proanthocyanidins (53.34 1.58 PE/g), displayed potent radical scavenging activities chemical-based assays. In cells, pretreatment restored balance endogenous antioxidant defense disrupted by t-BHP, as evidenced significant reductions ROS generation lipid peroxidation levels, along with enhanced antioxidants. Specifically, 25 μg/mL reduced levels 53.03%, decreased MDA content 78.82%, superoxide dismutase (SOD) activity 12.42%, improved ratio glutathione (GSH) to oxidized (GSSG) 80.34% compared t-BHP group. Furthermore, rescued mitochondrial membrane collapse, inhibited cytochrome c (Cyt.c) release, prevented subsequent apoptotic death. Notably, neuroprotective efficacy comparable that edaravone, an approved drug. Mechanistic investigations combining network pharmacology experimental validation revealed PI3K/Akt/Nrf2 signaling pathway played pivotal role mediating PSE. Compared t-BHP-treated µg/mL significantly upregulated PI3K/Akt phosphorylation, expression Nrf2, downstream proteins heme oxygenase-1 (HO-1) NAD(P)H dehydrogenase quinone 1 (NQO1). Conclusions: Collectively, these findings demonstrate natural agent oxidative-related

Language: Английский

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