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Protective Effects of Hydroxysafflor Yellow A on β-Amyloid-Induced Neurotoxicity in PC12 Cells

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Abstract

The accumulation of extracellular amyloid-β peptide (Aβ) has been considered as one of the important causes of Alzheimer’s disease (AD), the most prevalent form of dementia. Hydroxysafflor yellow A (HSYA), a major active chemical component isolated from Carthamus tinctorius L., has been shown to possess neuroprotective actions in various ischemic models in vivo. The present study aimed to investigate the potential protective effect of HSYA against Aβ-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. The PC12 cells were pretreated with different concentrations (20, 40 and 80 μM) of HSYA for 2 h and then further treated with Aβ (20 μM) for 24 h. The results showed that Aβ could significantly decrease cell viability, glutathione level, mitochondrial membrane potential and the ratio of Bcl-2/Bax protein expression, while elevate the release of lactate dehydrogenase, the formation of DNA fragmentation, the levels of malondialdehyde and intracellular reactive oxygen species in PC12 cells. However, pretreatment with HSYA could effectively reverse these changes induced by Aβ in PC12 cells. Our experimental results demonstrate that HSYA may be a potential neuroprotective agent warranting further development for treatment of AD.

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Acknowledgments

We thank Mr. Yu-Feng Qiao for the generous donation of purified HSYA. This work was supported by grants from the Guangdong International Cooperation Projects in 2012, Guangdong Province, P.R. China (Project No. 2012B050300002), and International Cooperation Platform Construction for Chinese Medicine Innovation in Treating Cardiovascular and Metabolic Disease (No.2011B050300021).

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Correspondence to Zhi-Xiu Lin or Zi-Ren Su.

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Song-Zhi Kong and Yan-Fang Xian Contributed equally.

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Kong, SZ., Xian, YF., Ip, SP. et al. Protective Effects of Hydroxysafflor Yellow A on β-Amyloid-Induced Neurotoxicity in PC12 Cells. Neurochem Res 38, 951–960 (2013). https://doi.org/10.1007/s11064-013-1002-7

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  • DOI: https://doi.org/10.1007/s11064-013-1002-7

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