The objective of this study was to find the role of LncRNA SNHG12 in the regulation of hypertensive vascular endothelial injury. LncRNA SNHG12 and miR‐25‐3p expression were detected by quantitative RT‐PCR. Protein levels of Sirtuin 6 (SIRT6), endothelial cell (EC) senescence markers p16 and p21, and EC marker CD31 were measured by Western blot. The apoptosis of HUVECs was detected by flow cytometry. The binding between LncRNA SNHG12 and miR‐25‐3p was verified by dual luciferase reporter gene assay and RNA pull‐down assay. As a result, LncRNA SNHG12 was down‐regulated in aortic primary ECs isolated from Ang II‐induced hypertensive mice and 1 kidney/deoxycorticosterone acetate/salt‐induced hypertensive mice. In Ang II‐treated HUVECs, the expression level of SNHG12 was reduced and the overexpression of SNHG12 inhibited EC senescence markers p16 and p21 expressions, the apoptosis of HUVECs, and caspase‐3 activity. Further investigation confirmed that LncRNA SNHG12 bound to miR‐25‐3p, and negatively regulated miR‐25‐3p expression. MiR‐25‐3p directly targeted SIRT6 and negatively regulated SIRT6 expression. In addition, SNHG12 overexpression inhibited Ang II‐induced HUVECs injury through regulating miR‐25‐3p. Finally, in vivo experiments showed LncRNA SNHG12 overexpression alleviated vascular endothelial injury in Ang II‐induced hypertensive mice. In conclusion, LncRNA SNHG12 alleviates vascular endothelial injury induced by hypertension through miR‐25‐3p/SIRT6 pathway.

In the present study, we used the human umbilical vein endothelial cells (HUVECs) to investigate the anti-inflammatory effects and mechanism of taraxasterol on vascular inflammation. HUVECs were pre-treated with taraxasterol 1 h before lipopolysaccharide (LPS) treatment. The concentrations of TNF-α, IL-8, PGE2, and NO were measured. The expression of VCAM-1, ICAM-1, iNOS, COX-2, NF-κB, and LXRα was detected by western blot analysis. The results showed that taraxasterol not only reduced the production of TNF-α, IL-8, PGE2, and NO induced by LPS, but also reduced the expression of iNOS and COX-2. Taraxasterol also suppressed LPS-induced NF-κB activation and VCAM-1 and ICAM-1 expression. Furthermore, taraxasterol concentration-dependently increased the expression of LXRα. The inhibition of taraxasterol on TNF-α, IL-8, PGE2, and NO production can be reversed by geranylgeranyl diphosphate (GGPP, the LXRα inhibitor). Here, we found that taraxasterol inhibited vascular inflammation through activating LXRα.

Hypertension (HT) is a common chronic disease that often causes target-organ damage and severe complications, contributing to cardiovascular morbidity and mortality worldwide. Accumulating evidence suggests that inflammation plays a prominent role in the initiation and progression of HT. Multiple inflammatory biomarkers have been proposed to predict HT. Several new hematological parameters can reflect the inflammatory response and platelet activation. The major advantage of hematological parameters over conventional inflammatory markers is that they are relatively inexpensive and easily obtained from routine blood tests. Numerous studies have investigated several hematological parameters for their utility as predictive biomarkers for the diagnosis and prognosis of HT. Among them, the neutrophil to lymphocyte ratio (NLR), monocyte to high density lipoprotein cholesterol ratio (MHR), red cell distribution width (RDW), platelet to lymphocyte ratio (PLR), mean platelet volume (MPV), platelet distribution width (PDW), and systemic immune-inflammation index (SII) have recently received attention. We searched PubMed and Embase databases (up to September 18, 2022) to assess the relationships between hematological parameters and HT. This review discusses the diagnostic and prognostic value of these hematological parameters in HT, providing an important basis for early screening, risk stratification, and optimal management of hypertensive patients.