baohuoside-i and Diabetes-Mellitus

The aim of the study was to investigate whether miR-126, a regulator of MAPK signaling via targeting sprouty-related EVH1 domain-containing protein 1 (. Primary hCECs were isolated and divided into three groups, normal control, diabetes mellitus (DM), and DM treated with ICA II. The cell proliferation and migration abilities of the hCECs were examined. The expression levels of endothelial-related microRNAs and relative target mRNAs (. hCECs induced with glucose plus advanced glycation end product-BSA showed a significant decrease in endothelial nitric oxide synthase, Ki-67, and miR-126 expression; a downregulated cell migration ability and an increased receptor for advanced glycation end products level. ICA II could partially reverse these changes.. ICA II could ameliorate endothelial dysfunction by regulating the MAPK pathway via miR-126/SPRED1 in hCECs exposed to a diabetic-like environment, and ICA II might be a protective agent for endothelial function in diabetic ED.

Topics: Adaptor Proteins, Signal Transducing; Case-Control Studies; Cell Movement; Cell Proliferation; Cells, Cultured; Cellular Microenvironment; Diabetes Mellitus; Dose-Response Relationship, Drug; Endothelial Cells; Endothelium, Vascular; Enzyme Activation; Flavonoids; Glucose; Glycation End Products, Advanced; Humans; Hypoglycemic Agents; Intracellular Signaling Peptides and Proteins; Male; Membrane Proteins; MicroRNAs; Mitogen-Activated Protein Kinases; Nitric Oxide Synthase Type III; Receptor for Advanced Glycation End Products; RNA, Messenger; Serum Albumin, Bovine; Signal Transduction