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Sodium tanshinone IIA sulfonate protects against Aβ-induced cell toxicity through regulating Aβ process
Da-Peng Zhang1, Xin-Yi Lu2, Si-Chen He3
1The First Affiliated Hospital of Guangzhou Medical University, 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.
Insights
Sodium tanshinone IIA sulfonate (STS) protects against Alzheimer's disease (AD) by reducing amyloid-beta (Aβ) toxicity and inflammation. This compound modulates Aβ generation and degradation, showing promise for AD treatment.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Alzheimer's disease (AD) is a neurodegenerative disorder characterized by amyloid-beta (Aβ) plaque accumulation.
- The precise mechanisms underlying Aβ-induced neurotoxicity and potential therapeutic interventions remain areas of active research.
Purpose of the Study:
- To investigate the neuroprotective effects of Sodium tanshinone IIA sulfonate (STS) against Aβ-induced toxicity in vitro.
- To elucidate the underlying molecular mechanisms of STS's action in Alzheimer's disease models.
Main Methods:
- Utilized two in vitro models: Aβ-treated SH-SY5Y cells and SH-SY5Y human neuroblastoma cells transfected with APPsw.
- Assessed cell viability, oxidative stress markers (ROS, MDA, NO, iNOS, SOD, GPx), inflammatory factors (IL-1β, IL-6, TNF-α), Aβ levels, and secretase activities (ADAM10, BACE1).
- Employed techniques including Western blot, ELISA, and quantitative PCR (qPCR).
Main Results:
- STS demonstrated dose-dependent protection against Aβ-induced cell toxicity.
- STS reduced oxidative stress and inflammation markers.
- STS upregulated neprilysin and insulin-degrading enzyme, decreased Aβ levels, increased α-secretase (ADAM10) activity, and decreased β-secretase (BACE1) activity.
Conclusions:
- STS protects against Aβ-induced neurotoxicity by modulating Aβ generation and degradation pathways.
- STS exhibits potential as a therapeutic candidate for Alzheimer's disease treatment.
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