Abstract
Purpose: In type 2 diabetes, palmitic acid could damage vessels and induce insulin resistance. This present in vitro study evaluates the possible role of Spatholobus suberectus (FSS) extract in diabetes.Methods: Human HUVECc cells were treated with palmitic acid, palmitic acid and Spatholobus suberectus extract. MALAT1 overexpression plasmid (pcDNA-MALAT1) and blank vector were transfected into the cells using lipofectamine 2000. RT-qPCR assay was used to evaluated the expression changes of lncRNA, VEGFR2 and VEGFA in the cells as well as Epithelial-Mesenchymal Transition (EMT) biomarkers and apoptosis. CCK-8 was used to detect cell viabilities of HUVECs. Expressions of proteins in VEGF signaling pathway were analyzed using Western Blot.Results: LncRNA MALAT1 had high expression in diabetes-like cells and suppressed proliferation and EMT but promoted apoptosis. The SS extract promoted proliferation and EMT and repressed apoptosis in diabetes-like HUVECs cells. The promotion of apoptosis by LncRNA MALAT1, inhibition of apoptosis and regulated functions of diabetes-like HUVECs cells by SS extract occurred via the VEGF signaling pathwayConclusion: SS extract might contribute to survival of cells by inhibiting MALAT1 via VEGF signaling pathway in vitro, suggesting FSF might be a potential therapeutic agent in the treatment of diabetes.
 Keywords: flavone of Spatholobus suberectus, diabetes, vascular endothelial cell, LncRNA MALAT1
Highlights
Diabetes is a metabolic disease with damaged functions of pancreatic islet or insulin resistance that may be caused by genetic factors, immune disorders, microbial infection or obesity, etc [1]
When the expressions of lncRNA MALAT1 was evaluated in normal human HUVECs and palmitic acid induced HUVECs, lncRNA MALAT1 expressed higher in diabetes-like HUVECs (Figure 1A) when compared to normal cells
The results of CCK-8 showed that overexpressed lncRNA MALAT1 significantly reduced cell viability of induced HUVECs (Figure 1C)
Summary
Diabetes is a metabolic disease with damaged functions of pancreatic islet or insulin resistance that may be caused by genetic factors, immune disorders, microbial infection or obesity, etc [1]. The high morbidity and mortality of cardiovascular diseases caused by diabetes has become a serious problem that threatens human health. Patients with diabetes often have abnormal angiogenesis, which is the main factor of diabetic cardiovascular complications [3]. Vascular endothelial growth factor (VEGF) plays an important role in regulating angiogenesis in physiological and pathological conditions [4]. VEGF and its receptor vascular endothelial factor receptor-2 (VEGFR-2) axis are affected by diabetes to militate growth of cardiovascular diseases [5]. It can influence to insulin signaling pathway, causing dysfunctions of vascular endothelial cells and leading to insulinresistant state [6]
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