Fermented Chinese Formula Shuan-Tong-Ling Protects Brain Microvascular Endothelial Cells against Oxidative Stress Injury.

Lingjing Tan,Weifeng Huang,Songbai Yang,Zhigang Mei,Jinfeng Wang,Xiang Zhang,Xiaoli Li

doi:10.1155/2016/5154290

Abstract

Fermented Chinese formula Shuan-Tong-Ling (STL), composed of fourteen medicinal herbs, was an experiential formula by Dr. Zhigang Mei for treating vascular encephalopathy, but the underlying mechanisms remained unknown. In this study, we aimed to investigate the protective effects of fermented STL on hydrogen peroxide- (H2O2-) induced injury in rat brain microvascular endothelial cells (BMECs) and the possible mechanisms. Cultured BMECs were treated with H2O2, STL, or nicotinamide (NAM, a SIRT1 inhibitor). Then, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay was employed to detect cell proliferation and senescence-associated beta-galactosidase (SA-β-gal) was used to examine cell senescence. Cell nuclei were observed by 4′,6-diamidino-2-phenylindole. Additionally, changes in reactive oxygen species (ROS), superoxide dismutase (SOD), and glutathione (GSH) levels were measured. Expression of SIRT1, p21, and PGC-1α was determined by western blot. Cell proliferation significantly increased with STL treatment in a dose-dependent manner. H2O2 treatment could intensify cell senescence and nuclei splitting or pyknosis. With STL treatment, the reduced ROS level was accompanied by increased SOD and GSH activity. Further assays showed upregulation of SIRT1 and PGC-1α and downregulation of p21 after STL treatment. The results revealed that STL could protect BMECs against oxidative stress injury at least partially through the SIRT1 pathway.

Highlights

During normal physiological conditions, reactive oxygen species (ROS) are produced at low levels and are scavenged by endogenous antioxidant systems that include superoxide dismutase (SOD), glutathione peroxidase, catalase, and small-molecule substances such as vitamins C and E [1]
This study focused on determining the efficacy of STL on the H2O2-induced injury in brain microvascular endothelial cells (BMECs) and exploring the possible mechanisms
The present study suggested that STL could attenuate the pathogenic processes of H2O2-induced oxidative stress injury in rat brain microvascular endothelial cells (BMECs) by reducing H2O2-induced increase in the levels of intracellular

Summary

Introduction

Reactive oxygen species (ROS) are produced at low levels and are scavenged by endogenous antioxidant systems that include superoxide dismutase (SOD), glutathione peroxidase, catalase, and small-molecule substances such as vitamins C and E [1]. Abundant accumulation of ROS may partially account for the pathogenesis of vascular diseases such as atherosclerosis, hypertension, stroke, neurodegenerative diseases, diabetes, and aging [2, 3]. It is strongly associated with endothelial dysfunction development such as endothelial injury, mitochondrial damage, inflammation, autophagy, apoptosis, and aging [4,5,6,7]. As a member of the brain microvascular wall, brain microvascular endothelial cells (BMECs) are the most important part of the blood-brain barrier [9] and participate in regulating vascular tone, blood fluidity and adhesiveness, and normal blood circulation [10].

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