Ischemia stroke is thought to be one of vascular risks associated with neurodegenerative diseases, such as Alzheimer's disease (AD). Hydroxysafflor yellow A (HSYA) has been reported to protect against stroke… Click to show full abstract
Ischemia stroke is thought to be one of vascular risks associated with neurodegenerative diseases, such as Alzheimer's disease (AD). Hydroxysafflor yellow A (HSYA) has been reported to protect against stroke and AD, while the underlying mechanism remains unclear. In this study, SH-SY5Y cell model treated with oxygen glucose deprivation/reperfusion (OGD/R) was used to explore the potential mechanism of HSYA. Results from CCK-8 showed that 10μM HSYA restored the cell viability after OGD 2 h/R 24 h. HSYA reduced the levels of malondialdehyde and ROS, while improved the levels of superoxide dismutase and glutathione peroxidase. Furthermore, apoptosis was inhibited and the expression of brain-derived neurotrophic factor was improved after HSYA treatment. In addition, the expression levels of amyloid-β peptides (Aβ) and BACE1 were decreased by HSYA, as well as the expression levels of binding immunoglobulin heavy chain protein, PKR-like ER kinase pathway and activating transcription factor 6 pathway, while the expression level of protein disulfide isomerase was increased. Based on these results, HSYA might reduce Aβ toxicity after OGD/R by interfering with apoptosis, oxidation, and neurotrophic factors, as well as relieving endoplasmic reticulum stress.
               
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