ArticleNeurotoxicity research2022
A Pretreatment with Isoorientin Attenuates Redox Disruption, Mitochondrial Impairment, and Inflammation Caused by Chlorpyrifos in a Dopaminergic Cell Line: Involvement of the Nrf2/HO-1 Axis.
Article in Neurotoxicity research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Evaluation of an Integrated In Silico-In Vitro Pipeline for Predicting Mitochondrial Complex I-Mediated Neurotoxicity of Chlorpyrifos.Neurotoxicity research · 2026Article
- Umbelliferone reverses neuronal damage induced by chronic Chlorpyrifos exposure via suppressing NF-κB/STAT3/NLRP3 and boosting Keap-1/Nrf2/HO-1 signals.Metabolic brain disease · 2025Article
- Exploring the therapeutic potential of isoorientin in the treatment of osteoporosis: a study using network pharmacology and experimental validation.Molecular medicine (Cambridge, Mass.) · 2024Article
- Berberine alleviates chlorpyrifos-induced nephrotoxicity in rats via modulation of Nrf2/HO-1 axis.Heliyon · 2024Article
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5 authors at 2 institutions in 1 country.
Funding
Abstract
The C-glucosyl flavone isoorientin (ISO) is obtained by humans from the diet and exhibits several cytoprotective effects, as demonstrated in different experimental models. However, it was not previously shown whether ISO would be able to prevent mitochondrial impairment in cells exposed to a chemical stressor. Thus, we treated the human neuroblastoma SH-SY5Y cells with ISO (0.5-20 µM) for 18 h before a challenge with chlorpyrifos (CPF) at 100 µM for additional 24 h. We observed that ISO prevented the CPF-induced lipid peroxidation and protein carbonylation and nitration in the membranes of mitochondria extracted from CPF-treated cells. ISO also attenuated the CPF-elicited increase in the production of reactive species in this experimental model. Moreover, ISO prevented the CPF-induced disruption in the activity of components of the oxidative phosphorylation (OXPHOS) system in the SH-SY5Y cells. ISO also promoted an anti-inflammatory action in the cells exposed to CPF. CPF caused a decrease in the activity of the enzyme heme oxygenase-1 (HO-1), a cytoprotective agent. On the other hand, ISO upregulated HO-1 activity in SH-SY5Y cells. Inhibition of HO-1 by zinc protoporphyrin-IX (ZnPP-IX) suppressed the cytoprotection induced by ISO in the CPF-treated cells. Besides, silencing of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) abolished the ISO-induced HO-1 upregulation and mitochondrial benefits induced by this flavone on the CPF-challenged cells. Thus, ISO protected mitochondria of the CPF-treated cells by an Nrf2/HO-1-dependent fashion in the SH-SY5Y cells.
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