Hyperhomocysteinemia and increased red cell distribution width (RDW) are associated with a higher possibility of adverse clinical outcomes of hypertension. The study aims to validate the effect of homocysteine (Hcy) and RDW on cardiovascular events (CVE) and investigate whether RDW is independently associated with serum Hcy in patients with essential hypertension (EH). The study reviewed 804 patients with newly diagnosed EH in our hospital. The clinical characteristics and laboratory results of all subjects were grouped according to the presence/absence of CVE. Patients in the CVE group had higher RDW and Hcy, as compared to the patients in the no CVE group. Multiple Cox regression analysis demonstrated that both RDW (HR = 1.24, 95% CI =1.02–1.56, P = 0.002) and Hcy (HR = 1.37, 95% CI = 1.02–1.80, P < 0.001) resulted significantly related to the CVE. Subsequent analysis found that patients with high RDW had higher Hcy levels as compared with those with low RDW (P = 0.007). Although Pearson's correlation suggested that RDW was positively correlated with Hcy (r = 0.122, P = 0.028), no significant correlation was observed between RDW and Hcy (β = 0.15, p = 0.126) after adjusted for a series of potential confounders using multiple linear regression analysis. In conclusion, RDW is not correlated with Hcy in patients with EH. Both RDW and Hcy are independent risk factors for CVE in newly diagnostic EH and have the potential to improve risk stratification.

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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.