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BMC Neurosci. 2012 Dec 29;13:156. doi: 10.1186/1471-2202-13-156.

Astaxanthin protects against MPP(+)-induced oxidative stress in PC12 cells via the HO-1/NOX2 axis.

Author information

1
Department of Neurology, Fujian Institute of Geriatrics, The Affiliated Union Hospital of Fujian Medical University, 29 Xinquan Road, Fuzhou, Fujian 350001, China. unionqyye@163.com

Abstract

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.

PMID:
23272707
PMCID:
PMC3541259
DOI:
10.1186/1471-2202-13-156
[Indexed for MEDLINE]
Free PMC Article

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