Why the study?
Endothelial barrier disruption and glycocalyx damage are key in diabetic vascular complications, motivating investigation into high-glucose effects on endothelial glycocalyx and the protective role of ginsenoside Rg1.
Does Ginsenoside Rg1 prevent high glucose-induced endothelial barrier dysfunction in human umbilical vein endothelial cells?
Does Ginsenoside Rg1 prevent high glucose-induced endothelial barrier dysfunction in human umbilical vein endothelial cells?
Ginsenoside Rg1 protects against high glucose-induced endothelial barrier dysfunction in vitro by preserving the endothelial glycocalyx and reducing heparanase expression.
Hypothesis-generating for Rg1 in diabetic endothelial dysfunction; leaves open clinical translation pending in vivo and human studies.
Disruption of the endothelial barrier is essential for vascular complications associated with diabetes mellitus, and damage to the endothelial glycocalyx has been demonstrated to participate in this process. Ginsenoside Rg1 (Rg1), the major active component isolated from Panax notoginseng, is widely applied for the protection against vascular injury. The present study aimed to analyze the effect of high glucose on endothelial barrier function and its association with endothelial glycocalyx in human umbilical vein endothelial cells (HUVECs), and explore the potential benefits of Rg1 in protecting endothelial barrier function from high glucose‑induced injury. The results indicated that high glucose induced a disorder of the endothelial glycocalyx and increased heparanase mRNA expression in HUVECs, which was reversed by Rg1 treatment. In addition, Rg1 treatment reduced transendothelial electrical resistance and transendothelial albumin passage after high‑glucose stimulation. The present study suggested that high glucose caused a disruption in the endothelial glycocalyx and increased heparanase expression, which finally resulted in endothelial barrier dysfunction in HUVECs. Of note, Rg1 has a protective effect on high glucose‑induced endothelial barrier dysfunction by attenuating the associated increase in heparanase expression.
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Zhu et al. (2019) studied this question.
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