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Sailuotong Prevents Hydrogen Peroxide (H(2)O(2))-Induced Injury in EA.hy926 Cells

Sailuotong (SLT) is a standardised three-herb formulation consisting of Panax ginseng, Ginkgo biloba, and Crocus sativus designed for the management of vascular dementia. While the latest clinical trials have demonstrated beneficial effects of SLT in vascular dementia, the underlying cellular mechan...

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Detalles Bibliográficos
Autores principales: Seto, Sai Wang, Chang, Dennis, Ko, Wai Man, Zhou, Xian, Kiat, Hosen, Bensoussan, Alan, Lee, Simon M. Y., Hoi, Maggie P. M., Steiner, Genevieve Z., Liu, Jianxun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5297729/
https://www.ncbi.nlm.nih.gov/pubmed/28067784
http://dx.doi.org/10.3390/ijms18010095
Descripción
Sumario:Sailuotong (SLT) is a standardised three-herb formulation consisting of Panax ginseng, Ginkgo biloba, and Crocus sativus designed for the management of vascular dementia. While the latest clinical trials have demonstrated beneficial effects of SLT in vascular dementia, the underlying cellular mechanisms have not been fully explored. The aim of this study was to assess the ability and mechanisms of SLT to act against hydrogen peroxide (H(2)O(2))-induced oxidative damage in cultured human vascular endothelial cells (EAhy926). SLT (1–50 µg/mL) significantly suppressed the H(2)O(2)-induced cell death and abolished the H(2)O(2)-induced reactive oxygen species (ROS) generation in a concentration-dependent manner. Similarly, H(2)O(2) (0.5 mM; 24 h) caused a ~2-fold increase in lactate dehydrogenase (LDH) release from the EA.hy926 cells which were significantly suppressed by SLT (1–50 µg/mL) in a concentration-dependent manner. Incubation of SLT (50 µg/mL) increased superoxide dismutase (SOD) activity and suppressed the H(2)O(2)-enhanced Bax/Bcl-2 ratio and cleaved caspase-3 expression. In conclusion, our results suggest that SLT protects EA.hy916 cells against H(2)O(2)-mediated injury via direct reduction of intracellular ROS generation and an increase in SOD activity. These protective effects are closely associated with the inhibition of the apoptotic death cascade via the suppression of caspase-3 activation and reduction of Bax/Bcl-2 ratio, thereby indicating a potential mechanism of action for the clinical effects observed.