1. Academic Validation
  2. Sodium tanshinone IIA sulfonate protects against Aβ-induced cell toxicity through regulating Aβ process

Sodium tanshinone IIA sulfonate protects against Aβ-induced cell toxicity through regulating Aβ process

  • J Cell Mol Med. 2020 Mar;24(6):3328-3335. doi: 10.1111/jcmm.15006.
Da-Peng Zhang 1 Xin-Yi Lu 2 Si-Chen He 3 Wan-Yan Li 1 Ran Ao 1 Feona Chung-Yin Leung 4 Zhi-Min Zhang 1 Qu-Bo Chen 2 Shi-Jie Zhang 5
Affiliations

Affiliations

  • 1 The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
  • 2 Biological Resource Center, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
  • 3 Department of Neurology, The People's Hospital of Baiyun District Guangzhou, Guangzhou, China.
  • 4 LKS Faculty of Medicine, School of Chinese Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
  • 5 Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
Abstract

Sodium tanshinone IIA sulfonate (STS) has been reported to prevent Alzheimer's disease (AD). However, the mechanism is still unknown. In this study, two in vitro models, Aβ-treated SH-SY5Y cells and SH-SY5Y human neuroblastoma cells transfected with APPsw (SH-SY5Y-APPsw cells), were employed to investigate the neuroprotective of STS. The results revealed that pretreatment with STS (1, 10 and 100 µmol/L) for 24 hours could protect against Aβ (10 µmol/L)-induced cell toxicity in a dose-dependent manner in the SH-SY5Y cells. Sodium tanshinone IIA sulfonate decreased the concentrations of Reactive Oxygen Species, malondialdehyde, NO and iNOS, while increased the activities of superoxide dismutase and Glutathione Peroxidase in the SH-SY5Y cells. Sodium tanshinone IIA sulfonate decreased the levels of inflammatory factors (IL-1β, IL-6 and TNF-α) in the SH-SY5Y cells. In addition, Western blot results revealed that the expressions of Neprilysin and insulin-degrading Enzyme were up-regulated in the SH-SY5Y cells after STS treatment. Furthermore, ELISA and Western blot results showed that STS could decrease the levels of Aβ. ELISA and qPCR results indicated that STS could increase α-secretase (ADAM10) activity and decrease β-secretase (BACE1) activity. In conclusion, STS could protect against Aβ-induced cell damage by modulating Aβ degration and generation. Sodium tanshinone IIA sulfonate could be a promising candidate for AD treatment.

Keywords

Aβ; Aβ degration; Aβ generation; sodium tanshinone IIA sulfonate.

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