RETRACTED: Baicalin relieves TNF-α-evoked injury in human aortic endothelial cells by up-regulation of miR-145 (Retracted Article)

Hypertension is recognized to be associated with low-grade inflammation. Baicalin (BAI) is reported to possess various pharmacological including anti-inflammatory activities. This research explored the molecular mechanism by which BAI functions in human aortic endothelial cells (HAECs). HAECs were pretreated with BAI. Cell viability, apoptosis, and expressions of crucial proteins were respectively evaluated using cell counting kit-8 assay, flow cytometry, and western blot. Productions of cytokines were respectively assessed employing quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay. Cell transfection was utilized to alter miR-145 expression. The expressions of proteins participated in JNK and p38MAPK pathways were analyzed utilizing western blot. TNF-alpha inducement successfully evoked inflammatory injury in HAECs, exhibiting as prominently suppressed viability, while facilitated apoptosis and productions of cytokines. However, BAI pretreatment significantly ameliorated TNF-alpha-triggered inflammatory injuries. Besides, miR-145 expression was markedly inhibited by TNF-alpha inducement, while notably elevated by BAI pretreatment. Although miR-145 overexpression had no significant influence on apoptosis, miR-145 silence observably reversed BAI pretreatment-evoked protective influences on TNF-alpha-induced HAECs, as well as the inhibited impacts on the levels of key proteins involved in JNK and p38MAPK pathways. This investigation illustrated that BAI relieved TNF-alpha-triggered injuries through upregulating miR-145 via suppressing JNK and p38MAPK pathways.