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Curcumin Alleviates β Amyloid-Induced Neurotoxicity in HT22 Cells via Upregulating SOD2

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Abstract

Curcumin protects neuronal cells exposed to β amyloid (Aβ); the mechanism, however, is still obscure. The aim of this study is to determine whether the type 2 superoxide dismutase (SOD2) mediates curcumin-induced protective effects in Aβ-treated neuronal cells. In this study, the HT22 neuronal cells were exposed to Aβ to imitate neuronal injury in Alzheimer’s disease (AD). After 24-h treatment, 10 μM Aβ decreased cell viability and mitochondrial functions, including mitochondrial complex activities and mitochondrial membrane potential (MMP), and also downregulated anti-oxidants SOD2, glutathione (GSH), and catalase (CAT) levels (P < 0.05), meanwhile, increased lactic dehydrogenase (LDH) release, apoptosis level, intracellular reactive oxygen species (ROS) and mitochondrial superoxide accumulation (P < 0.05). And, co-administration of 1 μM curcumin significantly reduced the Aβ-induced cell injury and oxidative damage above (P < 0.05). Downregulating SOD2 by using small interfering RNA (siRNA), however, significantly abolished the curcumin-induced protective and anti-oxidative effects in HT22 cells (P < 0.05); the scramble (SC)-siRNA did not cause marked effects on the curcumin-induced protective effects (P > 0.05). These findings showed that curcumin can alleviate Aβ-induced injury in neuronal cells, and SOD2 protein may mediate the neuroprotective effects.

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Funding

This work was supported by the National Nature Science Foundation of China (61773130), Natural Science Foundation of Guangdong Province, China (2016A030313613), and the Science and Technology Program of Guangzhou, China (201707010027).

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Correspondence to Bo Xu or Ji Jia.

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All procedures were approved by the Ethics Committee of the General Hospital of Southern Theatre of PLA.

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The authors declare that they have no conflict of interest.

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Du, S., Zhang, Y., Yang, J. et al. Curcumin Alleviates β Amyloid-Induced Neurotoxicity in HT22 Cells via Upregulating SOD2. J Mol Neurosci 67, 540–549 (2019). https://doi.org/10.1007/s12031-019-01267-2

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  • DOI: https://doi.org/10.1007/s12031-019-01267-2

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