ArticleCell biochemistry and biophysics2024
Isoquercitrin alleviates OGD/R-induced oxidative stress and impaired mitochondrial biogenesis in SH-SY5Y cells via the NRF1/TFAM pathway.
Article in Cell biochemistry and biophysics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Enhancement of content, purity and anti-myocardial ischemia-reperfusion injury activity of persimmon leaf flavonoids: Ultrasonic-assisted extraction, purification and related mechanism.Ultrasonics sonochemistry · 2026Article
- NEXN-AS1 Predicts the Occurrence of Post-Stroke Cognitive Impairment and Alleviates Inflammation and Oxidative Stress by Targeting the miR-92a-3p/NRF1 Axis : NEXN-AS1 Alleviates Inflammation and Oxidative Stress in PSCI.Neurochemical research · 2025Article
- Analysis of the Protective Mechanism of PGC-1α/NRF1/2/TFAM Pathway in Cortical Neuron Injury Induced by Oxidative Stress.Bulletin of experimental biology and medicine · 2025Article
- Role of mitochondrial metabolism in ischemic stroke and natural products intervention.Molecular biology reports · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
Isoquercitrin (ISO) is a traditional Chinese medicine extract, that has been found to possess potent neuroprotective properties. However, its precise role in the context of ischemic stroke (IS) remains to be fully elucidated. We constructed an in vitro model of IS induced by OGD/R in SH-SY5Y cells. Cell viability, the levels of oxidative stress-related indicators (8-OHDG, MDA, SOD, GSH, and GSH-Px), ROS, and mitochondrial membrane potential were measured by using detection kits. The protein levels of GPX1, SOD, Cytc were measured. The mRNA levels of mitochondrial biogenesis-related indicators (Cytb, CO1, ND2, ND5, and ND6), and mtDNA copy number were measured by RT-qPCR. ATP levels were measured. Molecular docking between ISO and NRF1, and Co-IP assay for NRF1 and TFAM interaction were performed. Expression of NRF1 and TFAM was evaluated. ISO treatment reversed the detrimental effects of OGD/R on cell viability, attenuated the elevation of oxidative stress markers, restored antioxidant levels, and alleviated the impairment of mitochondrial biogenesis in SH-SY5Y cells. ISO interacted with NRF1 and increased its expression along with TFAM. Silencing NRF1 reversed the protective effects of ISO, suggesting its involvement in mediating the neuroprotective effects of ISO. ISO alleviates oxidative stress and mitochondrial biogenesis damage induced by OGD/R in SH-SY5Y cells by upregulating the NRF1/TFAM pathway.
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