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

Autor:	Ma HH; Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.; Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China., Wen JR; Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.; Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China., Fang H; Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.; Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China., Su S; Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.; Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China.; College of Basic Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China., Wan C; Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.; Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China., Zhang C; Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.; Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China., Lu FM; Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.; Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China.; Department of Neurology, Henan University of Chinese Medicine, Zhengzhou, China., Fan LL; Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.; Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China.; Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China., Wu GL; Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.; Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China., Zhou ZY; Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.; Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China., Qiao LJ; Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.; Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China., Zhang SJ; Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.; Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China., Cai YF; Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.; Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China.
Jazyk:	angličtina
Zdroj:	Rejuvenation research [Rejuvenation Res] 2023 Apr; Vol. 26 (2), pp. 57-67. Date of Electronic Publication: 2023 Mar 20.
DOI:	10.1089/rej.2022.0054
Abstrakt:	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 μM 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-β peptides (Aβ) 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 Aβ toxicity after OGD/R by interfering with apoptosis, oxidation, and neurotrophic factors, as well as relieving ER stress.
Databáze:	MEDLINE
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