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- Title
Tanshinone IIA suppresses endoplasmic reticulum stress-induced apoptosis of high glucose-conditioned vascular endothelial cells by regulating microRNA-133/RAC-1 pathway.
- Authors
Lele Yang; Xiaofen Wu; Xiaoling Song; Decheng Pan
- Abstract
Cellular stress caused by abnormal accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER) is becoming a possible driver of cardiovascular diseases. The primary aim of our study was to explore Tanshinone IIA (Tan IIA)-induced protection against ER-induced apoptosis of human umbilical vein endothelial cells (HUVECs). HUVECs were treated with high glucose (HG), administrated with Tan IIA (2.5, 5, and 10 μM), and transfected with microRNA-133 (miR-133) mimic or inhibitor. Then cell viability was evaluated by MTT assay, the release of lactate dehydrogenase (LDH) was measured by detection kit, and ER stress was analyzed by Western blot measurement of ER stress-related indicators. Cell apoptosis was observed through flow cytometry and Western blot analysis of apoptosis-related markers. miR-133 and RAC-1 expressions in HUVECs were assessed. For HUVECs, HG inhibited cellular survival, promoted the release of LDH, apoptosis and ER stress, down-regulated miR-133, and up-regulated RAC-1. We demonstrated that Tan IIA reverted the damage of HG to HUVECs in a concentration-dependent manner. miR-133 could negatively regulate RAC-1 expression, and Tan IIA inhibited RAC-1 expression by elevating miR-133, thereby reducing the damage of HG to HUVECs. Tan IIA regulates miR133–RAC-1 axis to reduce the apoptosis caused by ER stress in HG-induced HUVECs, which could provide new insights for treating cardiovascular diseases.
- Subjects
ENDOPLASMIC reticulum; GLUCOSE; VASCULAR endothelial cells; MICRORNA; APOPTOSIS
- Publication
Quality Assurance & Safety of Crops & Foods, 2022, Vol 14, Issue 2, p47
- ISSN
1757-8361
- Publication type
Article
- DOI
10.15586/qas.v14i2.994