The Levels of TNF-α, Tissue Factor, and Coagulation Function in Rats with Pulmonary Hypertension and the Intervention Effect of Sildenafil Encapsulated by Targeted Nanocarriers

Abstract

Pulmonary hypertension (PAH) is a proliferative disease of pulmonary blood vessels, but the pathogenesis of pulmonary hypertension is still unclear. This article explores the role of tumor necrosis factor-α (TNF-α), tissue factor (TF), and coagulation function (CF) in the pathogenesis of PAH. PAH is often accompanied by vascular intima injury and muscular arterial media thickening. Coupled with the wide application of nanotargeted drugs in recent years, a targeted nanocarrier encapsulating sildenafil was prepared in this study. The particle size, PDI, zeta potential, drug loading, and encapsulation efficiency were 194.32 ± 17.31 nm , 0.28 ± 0.02 , − 6.34 ± 0.33 , 24.61%, and 70.52%. The monocrotaline PAH rat model was constructed, and it was found that the levels of TNF-α, TF, and CF in the peripheral blood of PAH rats were abnormally increased. 30 PAH rats were randomly divided into 5 groups and injected with saline (NS group), sildenafil (sildenafil group), target the nanoempty carrier (TNC-E group), ordinary nanocarrier encapsulated sildenafil (CNC-sildenafil group), and targeted nanocarrier encapsulate sildenafil (TNC-sildenafil group). Compared with the NS group, the mean pulmonary artery pressure in the TNC-sildenafil group was lower ( P < 0.05 ). Compared with the normal rat group, the pulmonary small blood vessel media thickness, TNF-α level, TF level, and the area of myocardial cells were increased in the NS group, sildenafil group, TNC-E group, and CNC-sildenafil group ( P < 0.05 ). Compared with the NS group, the pulmonary small blood vessel media thickness, myocardial cell area, and the levels of TNF-α and TF in the TNC-sildenafil group were reduced ( P < 0.05 ). Targeting nanocarrier encapsulation of sildenafil can obviously reduce the average pulmonary artery pressure in rats with pulmonary hypertension, improve pulmonary vascular media proliferation and myocardial hypertrophy, and restore the levels of TNF-α, TF, and CF to a normal state.

NF‐κB affected the serum levels of TNF‐α and IL‐1β via activation of the MAPK/NF‐κB signaling pathway in rat model of acute pulmonary microthromboembolism

“…TNF‐α can also promote thrombosis by promoting the shedding of protein C receptor, inhibiting the production of thrombomodulin, inducing complement activation, stimulating endothelial cells, and mononuclear phagocytes to produce tissue factors, resulting in an imbalance of the coagulation system 35 . Previous study showed that the elevated levels of serum TNF‐α were closely related to the pathophysiological process of PH 36 . And we present evidence for increased of serum TNF‐α in APMTE rats.…”

“…35 Previous study showed that the elevated levels of serum TNF-α were closely related to the pathophysiological process of PH. 36 And we present evidence for increased of serum TNF-α in APMTE rats. The results suggested TNF-α levels had important value for closely monitoring development of PH and antiinflammatory therapies may help achieve positive outcomes in PH.…”

Retracted: The Levels of TNF‐α, Tissue Factor, and Coagulation Function in Rats with Pulmonary Hypertension and the Intervention Effect of Sildenafil Encapsulated by Targeted Nanocarriers

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Peer-review manipulation …”

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [1]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process:…”