ABSTRACT
Previous studies have confirmed that exposure to particulate matter with a diameter of ≤2.5 µm (PM2.5) is associated with inflammation. PM2.5 decreases cardiac cell viability and increases apoptosis through overproduction of reactive oxygen species (ROS). In the present study, the role of PM2.5 in ECs was investigated in vitro. Human umbilical vein endothelial cells and human microvascular endothelial cells (ECs) were incubated with PM2.5 (100800 µg/ml) to investigate the effects of PM2.5 on EC viability, migration, tube formation and intracellular levels of ROS. Cell viability and cell apoptosis were determined by MTT assay and flow cytometry analysis. Cell migration was assessed using a Boyden chamber assay, and tube formation was determined by matrigel assay. Tumor necrosis factorα and interleukin8 levels were measured by ELISA, and ROS levels were assessed with 2',7'dichlorofluorescin diacetate. The results indicated that PM2.5 decreases EC viability and increases EC apoptosis in a concentrationdependent manner. PM2.5 also decreased EC tube formation in a dosedependent manner. The results also demonstrated that PM2.5 suppresses adhesion to EC extracellular matrix proteins. Furthermore, PM2.5 exposure significantly induced ROS generation, indicative of oxidative stress. Finally, it was demonstrated that PM2.5 decreased angiogenesis in vivo. These results suggested that repeated exposure to PM2.5 induces vascular inflammation.
Subject(s)
Air Pollutants/adverse effects , Cell Movement , Cell Survival , Endothelial Cells/cytology , Inflammation/etiology , Neovascularization, Physiologic , Particulate Matter/adverse effects , Cell Line , Endothelial Cells/immunology , Endothelial Cells/metabolism , Human Umbilical Vein Endothelial Cells , Humans , Inflammation/immunology , Inflammation/metabolism , Interleukin-8/immunology , Oxidative Stress , Particle Size , Tumor Necrosis Factor-alpha/immunologyABSTRACT
Xuebijing (XBJ) injection is a complex traditional Chinese prescription that has been widely used to treat sepsis in China. However, its underlying mechanisms on sepsis still remain uninvestigated. In this study, 150 male Sprague Dawley rats were randomly divided into a normal control group, cecal ligation and puncture (CLP) group, CLP+XBJ group, and CLP+gibberellic acid group. Each of them contained 3 subgroups of different treatment periods (12, 24, and 48 hours after injection, respectively). The mRNA expression of HMGB1 in liver tissue of the 4 groups was calculated by the semiquantitative reverse-transcription polymerase chain reaction. The level of IL-6, IL-10, and TNF-α was determined by an enzyme-linked immunosorbent assay. Immunohistochemical analysis for HMGB1 showed the effect of XBJ on infiltration of inflammatory cells. The mRNA expression of HMGB1 in liver tissue in CLP+XBJ and CLP+gibberellic acid groups was lower than that in the CLP group. The levels of IL-6, IL-10, and TNF-α were decreased at the each monitored time point. All these results indicated that XBJ exhibits protective efficacy on sepsis by inhibiting the expression of HMGB1.