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Published on: November 18, 2022
Astaxanthin suppresses MPP(+)-induced oxidative damage in PC12 cells through a Sp1/NR1 signaling pathway
Qinyong Ye1, Xiaodong Zhang, Bixia Huang
1Department of Neurology, Fujian Institute of Geriatrics, The Affiliated Union Hospital of Fujian Medical University, 29 Xinquan Road, Fuzhou, Fujian 350001, China. unionqyye@163.com
Objective:
To investigate astaxanthin (ATX) neuroprotection, and its mechanism, on a 1-methyl-4-phenyl-pyridine ion (MPP+)-induced cell model of Parkinson's disease.
Methods:
Mature, differentiated PC12 cells treated with MPP+ were used as an in vitro cell model. The MTT assay was used to investigate cell viability after ATX treatment, and western blot analysis was used to observe Sp1 (activated transcription factor 1) and NR1 (NMDA receptor subunit 1) protein expression, real-time PCR was used to monitor Sp1 and NR1 mRNA, and cell immunofluorescence was used to determine the location of Sp1 and NR1 protein and the nuclear translocation of Sp1.
Results:
PC12 cell viability was significantly reduced by MPP+ treatment. The expression of Sp1 and NR1 mRNA and protein were increased compared with the control (p < 0.01). Following co-treatment with ATX and MPP+, cell viability was significantly increased, and Sp1 and NR1 mRNA and protein were decreased, compared with the MPP+ groups (p < 0.01). In addition, mithracycin A protected PC12 cells from oxidative stress caused by MPP+ by specifically inhibiting the expression of Sp1. Moreover, cell immunofluorescence revealed that ATX could suppress Sp1 nuclear transfer.
Conclusion:
ATX inhibited oxidative stress induced by MPP+ in PC12 cells, via the SP1/NR1 signaling pathway.
Insights
Astaxanthin (ATX) protects against Parkinson's disease models by reducing oxidative stress. It inhibits the SP1/NR1 pathway, offering neuroprotection in MPP+-treated cells.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Parkinson's disease is a neurodegenerative disorder.
- 1-methyl-4-phenyl-pyridine ion (MPP+) is used to create cell models of Parkinson's disease.
- Oxidative stress plays a key role in Parkinson's disease pathogenesis.
Purpose of the Study:
- To investigate the neuroprotective effects of astaxanthin (ATX) in an MPP+-induced Parkinson's disease cell model.
- To elucidate the underlying mechanism of ATX neuroprotection, focusing on the SP1/NR1 signaling pathway.
Main Methods:
- PC12 cells were treated with MPP+ to establish an in vitro Parkinson's disease model.
- Cell viability was assessed using the MTT assay.
- Protein and mRNA expression of Sp1 and NR1 were analyzed via Western blot and real-time PCR, respectively.
- Cell immunofluorescence was employed to track Sp1 and NR1 localization and Sp1 nuclear translocation.
Main Results:
- MPP+ treatment significantly reduced PC12 cell viability and increased Sp1 and NR1 expression.
- Co-treatment with ATX and MPP+ significantly increased cell viability and decreased Sp1 and NR1 expression.
- ATX treatment suppressed Sp1 nuclear translocation, indicating inhibition of the SP1/NR1 pathway.
- Mithracycin A, an Sp1 inhibitor, demonstrated protective effects against MPP+-induced oxidative stress.
Conclusions:
- Astaxanthin (ATX) exhibits significant neuroprotective effects in an MPP+-induced Parkinson's disease cell model.
- ATX exerts its neuroprotective action by inhibiting oxidative stress via the SP1/NR1 signaling pathway.
