Guo Y.,Sourthern Medical University |
Guo Y.,Beijing Key Laboratory of Pediatric Organ Failure |
Guo Y.,Inner Mongolia University |
Chai Q.,Inner Mongolia Peoples Hospital |
And 5 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2015
Autoimmune disease systemic lupus erythematosus (SLE) is associated with increased expression of pro-inflammatory cytokines such as interferons (IFNs) and specific interleukins (ILs), which are induced by toll-like receptors (TLRs). The present study aimed to examine the serum levels of cytokines, the activation of TLR-7 and TLR-8 of peripheral blood mononuclear cells (PBMCs) from pediatric SLE patients, and to investigate the response of those PBMCs to viral RNA via the TLR-7 and TLR-8 signaling. Results demonstrated that pediatric SLE patients had increased serum concentrations of interleukin (IL)-1β, IL-6, IL-8, IL-10, and IFN-α, and promoted activation of TLR-7 and TLR-8, compared to control subjects. Moreover, the peripheral blood mononuclear cells (PBMCs) from pediatric SLE patients were more sensitive to the stimulation by the transfection with viral RNA from influenza virus, with a promoted activation of TLR-7 and TLR-8 signaling. In conclusion, pro-inflammatory cytokines, such as IL-1β, IL-6, IL-8, IL-10, and IFN-α were promoted in pediatric SLE patients, with an increased activation of TLR-7 and TLR- 8 to the stimuli, such as virus infection. It implies the TLR-7 and TLR-8 activation by virus infection might play an important role in the pathogenesis of pediatric SLE. © 2015 E-Century Publishing Corporation. All rights reserved.
Shi M.-Q.,Beijing Key Laboratory of Pediatric Organ Failure |
Shi M.-Q.,PLA Fourth Military Medical University |
Su F.-F.,PLA Fourth Military Medical University |
Xu X.,Beijing Key Laboratory of Pediatric Organ Failure |
And 7 more authors.
Molecular Medicine Reports | Year: 2016
Patients with essential hypertension undergo endothelial dysfunction, particularly in the conduit arteries. Cilostazol, a type III phosphodiesterase inhibitor, serves a role in the inhibition of platelet aggregation and it is widely used in the treatment of peripheral vascular diseases. Previous studies have suggested that cilostazol suppresses endothelial dysfunction; however, it remains unknown whether cilostazol protects the endothelial function in essential hypertension. The aim of the present study was to investigate whether, and how, cilostazol suppresses angiotensin II (angII)-induced endothelial dysfunction. Human umbilical vein endothelial cells (HUVECs) and Sprague Dawley rats were exposed to angII and treated with cilostazol. Endothelial cell apoptosis and function, nitric oxide and superoxide production, phosphorylation (p) of Akt, and caspase-3 protein expression levels were investigated. AngII exposure resulted in the apoptosis of endothelial cells in vitro and in vivo. In vitro, cilostazol significantly suppressed the angII-induced apoptosis of HUVECs; however, this effect was reduced in the presence of LY294002, a phosphoinositide 3 kinase (PI3K) inhibitor. Furthermore, cilostazol suppressed the angII-induced p-Akt downregulation and cleaved caspase-3 upregulation. These effects were also alleviated by LY294002. In vivo, cilostazol suppressed the angII-induced endothelial cell apoptosis and dysfunction. Cilostazol was also demonstrated to partially reduced the angII-induced increase in superoxide production. The results of the present study suggested that cilostazol suppresses endothelial apoptosis and dysfunction by modulating the PI3K/Akt pathway.