Retracted: Baicalin relieves TNF‐α‐evoked injury in human aortic endothelial cells by up‐regulation of miR‐145

Abstract

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‐α 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‐α‐triggered inflammatory injuries. Besides, miR‐145 expression was markedly inhibited by TNF‐α 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‐α‐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‐α‐triggered injuries through upregulating miR‐145 via suppressing JNK and p38MAPK pathways.

Effect of miR-145 on intracardiac thrombosis in patients with rheumatic heart disease complicated with atrial fibrillation: A retrospective analysis

“…[24] TNF-α treatment can significantly induced human aortic endothelial cells to release inflammatory cytokines, including IL-6 and IL-8, while reducing the expression of miR-145. [25] In this study, we found that the expression of miR-145 decreased in RHD patients, especially in TH group. Interestingly, we found that miR-145 was negatively correlated with LAD, IL-6 level, and D-D level, respectively, suggesting that miR-145 may be involved in the pathogenesis of RHD, and the significant decrease of miR-145 expression can predict intracardiac thrombosis in patients with RHD.…”

Regulatory Mechanisms of Baicalin in Cardiovascular Diseases: A Review

“…In vivo, experimental data confirmed that baicalin forcefully lowered the blood pressure partly via decreasing the serum levels of high-sensitivity CRP, IL-6 and IL-1b in spontaneously hypertensive rats (SHRs) (Wu et al, 2019). Similarly, another vitro study showed that baicalin extenuated contents of TNF-a by altering miR-145 expression and significantly ameliorating TNF-a inflammatory injuries in human aortic endothelial cells (HAECs) (Li et al, 2020). With the popularization of the Holistic concept, numerous studies have revealed that a damage in the intestinal barrier, is considered as a critical role in the pathogenesis of hypertension primarily by exacerbating the development of chronic low-grade inflammation (Santisteban et al, 2017;Jaworska et al, 2017).…”

Identification of miR‑145 as a regulator of the cardiomyocyte inflammatory response and oxidative stress under hyperglycemia

“…Geniposide protects H9c2 cells against lipopolysaccharide (LPS)-induced apoptosis and inflammation by regulating miR-145 expression and the MEK/ERK signaling pathway (9). In human aortic endothelial cells, TNF-α treatment markedly induced the release of inflammatory cytokines, including monocyte chemoattractant protein-1 (MCP-1), IL-6 and IL-8, whilst decreasing the expression of miR-145 (10). Moreover, He et al (11) demonstrated that LPS treatment markedly elevated TNF-α levels, which strongly inhibited miR-145 expression under hyperglycemic conditions.…”