Hydroxysafflor Yellow A Exerts Neuroprotective Effect by Reducing Aβ Toxicity Through Inhibiting Endoplasmic Reticulum Stress in Oxygen-Glucose Deprivation/Reperfusion Cell Model

作者：Ma, Hui-Han; Wen, Jun-Ru; Fang, Hao; Su, Shan; Wan, Can; Zhang, Chao; Lu, Fang-Mei; Fan, Ling-Ling; Wu, Guang-Liang; Zhou, Zi-Yi; Qiao, Li-Jun; Zhang, Shi-Jie^*; Cai, Ye-Feng^*

来源：REJUVENATION RESEARCH, 2023, 26(2): 57-67.

DOI：10.1089/rej.2022.0054

• oxygen-glucose deprivation/reperfusion
• hydroxysafflor yellow A
• amyloid-beta
• endoplasmic reticulum stress

Ischemia stroke is thought to be one of the 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 cell counting kit-8 (CCK-8) showed that 10 mu M HSYA restored the cell viability after OGD 2 hours/R 24 hours. HSYA reduced the levels of malondialdehyde and reactive oxygen species, 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-beta peptides (A beta) and BACE1 were decreased by HSYA, as well as the expression levels of binding immunoglobulin heavy chain protein, PKR-like endoplasmic reticulum (ER) kinase pathway, and activating transcription factor 6 pathway, whereas the expression level of protein disulfide isomerase was increased. Based on these results, HSYA might reduce A beta toxicity after OGD/R by interfering with apoptosis, oxidation, and neurotrophic factors, as well as relieving ER stress.

• 单位
  广州中医药大学; 广东省人民医院