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.
Highlights
Alzheimer's disease (AD) is increasingly severe in this century.[1,2] The clinical characteristics of AD are deficiencies in cognition.[3]
Some evidence suggests that overproduction of or reduced clearance of Aβ is occurred in the process of AD, which leading to the formation of Aβ plaques.[6,7]
Two in vitro models, Aβ-treated SH-SY5Y cells and SH-SY5Y human neuroblastoma cells transfected with APPsw (SHSY5Y-APPsw cells), were employed to investigate the neuroprotective of Sodium tanshinone IIA sulfonate (STS)
Summary
Alzheimer's disease (AD) is increasingly severe in this century.[1,2] The clinical characteristics of AD are deficiencies in cognition.[3]. A large number of studies have shown that STS could protect against cardiovascular diseases.[12,13,14,15] Besides the well-known cardioprotective effect, STS possesses neuroprotective activity against neural dysfunction.[16,17,18] Previous studies suggested that STS have some pharmacological actions, such as anti-oxidative stress,[19,20] anti-inflammation.[13,21] STS has not yet been reported to have any Aβ-regulation effect. Considering during AD process, Aβ aggregation can damage and cause neuronal death by inducing oxidative stress and neuroinflammation.[22,23] it was hypothesized that STS could display the neuroprotective effects through modulating Aβ process. The cells were collected to detect the level of MDA by using the kit (Nianjing Jiancheng Bioengineering Institute) according to the manufacturer's instructions. The cells were collected to detect the activities of SOD and GSH-Px by using the kits (Nianjing Jiancheng Bioengineering Institute) according to the manufacturer's instructions
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