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Published on: November 18, 2022
Astaxanthin protects against MPP(+)-induced oxidative stress in PC12 cells via the HO-1/NOX2 axis
Qinyong Ye1, Bixia Huang, Xiaodong Zhang
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
Background:
Although the etiology of PD remains unclear, increasing evidence has shown that oxidative stress plays an important role in its pathogenesis and that of other neurodegenerative disorders. NOX2, a cytochrome subunit of NOX, transports electrons across the plasma membrane to generate ROS, leading to physiological and pathological processes. Heme oxygenase-1 (HO-1) can be rapidly induced by oxidative stress and other noxious stimuli in the brain or other tissues. Astaxanthin (ATX), a carotenoid with antioxidant properties, is 100-1000 times more effective than vitamin E. The present study investigated the neuroprotective effects of ATX on MPP(+)-induced oxidative stress in PC12 cells.
Results:
MPP(+) significantly decreased MTT levels in a concentration-dependent manner. Hemin, SnPPIX and ATX didn't exhibit any cytotoxic effects on PC12 cells. Pretreatment with ATX (5, 10, 20 μM), caused intracellular ROS production in the MPP(+) group to decrease by 13.06%, 22.13%, and 27.86%, respectively. MPP(+) increased NOX2, NRF2 and HO-1 protein expression compared with control (p < 0.05). Co-treatment with hemin or ATX suppressed NOX2 expression (p < 0.01), and greatly increased NRF2 and HO-1 expression (p < 0.01). MPP(+) treatment up-regulated both NOX2 (p < 0.01) and HO-1 (p < 0.01) mRNA levels. Co-treatment with hemin or ATX significantly increased HO-1 mRNA levels (p < 0.01), and decreased NOX2 mRNA levels (p < 0.01). MPP(+) increased NOX2 and HO-1 expression with considerable fluorescence extending out from the perinuclear region toward the periphery; this was attenuated by DPI. Co-treatment with hemin or ATX significantly up-regulated HO-1 expression and decreased NOX2 expression with considerable fluorescence intensity (stronger than the control and MPP(+) groups).
Conclusions:
ATX suppresses MPP(+)-induced oxidative stress in PC12 cells via the HO-1/NOX2 axis. ATX should be strongly considered as a potential neuroprotectant and adjuvant therapy for patients with Parkinson's disease.
Insights
Astaxanthin (ATX) effectively reduces oxidative stress in Parkinson's disease models by modulating the heme oxygenase-1 (HO-1) and NADPH oxidase 2 (NOX2) pathways. This suggests ATX as a promising neuroprotective agent for Parkinson's disease treatment.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Oxidative stress is implicated in Parkinson's disease (PD) pathogenesis.
- NADPH oxidase 2 (NOX2) generates reactive oxygen species (ROS), contributing to cellular damage.
- Heme oxygenase-1 (HO-1) is an antioxidant enzyme induced by oxidative stress.
- Astaxanthin (ATX), a potent antioxidant, is investigated for neuroprotective effects.
Purpose of the Study:
- To investigate the neuroprotective effects of Astaxanthin (ATX) against MPP(+)-induced oxidative stress in PC12 cells.
- To elucidate the role of the HO-1/NOX2 axis in ATX-mediated neuroprotection.
Main Methods:
- PC12 cells were treated with MPP(+) to induce oxidative stress.
- Cells were pretreated with varying concentrations of ATX.
- Cell viability (MTT assay), intracellular ROS levels, and protein/mRNA expression of NOX2, NRF2, and HO-1 were assessed.
- Immunofluorescence was used to visualize NOX2 and HO-1 expression patterns.
Main Results:
- MPP(+) significantly reduced cell viability and increased ROS production.
- ATX pretreatment dose-dependently attenuated MPP(+)-induced ROS production and cell damage.
- ATX suppressed NOX2 expression while significantly upregulating NRF2 and HO-1 expression at both protein and mRNA levels.
- ATX treatment reversed the alterations in NOX2 and HO-1 expression patterns observed in MPP(+)-treated cells.
Conclusions:
- Astaxanthin (ATX) exerts neuroprotective effects against MPP(+)-induced oxidative stress in PC12 cells.
- The mechanism involves the modulation of the HO-1/NOX2 signaling pathway.
- ATX demonstrates potential as a neuroprotectant and adjuvant therapy for Parkinson's disease.
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