Effects of HSYA on the proliferation and apoptosis of MSCs exposed to hypoxic and serum deprivation conditions

As a primary active ingredient of safflor yellow, hydroxysafflor yellow A (HSYA) exhibits notable antioxidative and neuroprotective effects. The aim of the present study was to investigate the protective effects of HSYA in mesenchymal stem cells (MSCs) exposed to hypoxia (5% O ) and serum deprivatio...

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Bibliographic Details
Published in:Experimental and therapeutic medicine 2018-06, Vol.15 (6), p.5251-5260
Main Authors: Song, Xiaoqing, Su, Lining, Yin, Haifeng, Dai, Jin, Wei, Huiping
Format: Article
Language:English
Subjects:
Apoptosis
Cell proliferation
Chemical properties
Cytological research
Health aspects
Hypoxia
Laboratory animals
Medical research
Neurons
Phytochemicals
Proteins
Reactive oxygen species
Rodents
Safflower
Stem cells
Studies
Traumatic brain injury
Vascular endothelial growth factor
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Summary:As a primary active ingredient of safflor yellow, hydroxysafflor yellow A (HSYA) exhibits notable antioxidative and neuroprotective effects. The aim of the present study was to investigate the protective effects of HSYA in mesenchymal stem cells (MSCs) exposed to hypoxia (5% O ) and serum deprivation (H/SD), and to explore the mechanisms underlying HSYA-mediated protection. Under H/SD conditions, HSYA was applied to protect MSCs against injury. Cell viability, proliferation, apoptosis and reactive oxygen species (ROS) levels were determined using an 5-ethynyl-2'-deoxyuridine assay, MTT assay, Hoechst 33342/propidium iodide and 2',7'-dichlorodihydrofluorescein diacetate staining, respectively. The results revealed that 160 mg/l HSYA significantly reduced apoptosis and ROS levels compared with the H/SD group; however, HSYA demonstrated minimal effects on cell proliferation. A western blot assay demonstrated that HSYA reduced cleaved caspase-3 expression and cytC release from the mitochondria to the cytoplasm when compared with the H/SD group. In addition, western blotting and RT-qPCR analyses revealed that HSYA treatment significantly increased the expression of hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF). In conclusion, the results of the current study demonstrated that HSYA exerts protective effects against H/SD-induced apoptosis in MSCs potentially via activation of the HIF-1α/VEGF signaling pathway and stabilization of the mitochondrial membrane.
ISSN:1792-0981
1792-1015
DOI:10.3892/etm.2018.6125