Abstract
Oxidative stress plays an important role in the pathogenesis of endothelial dysfunction, which is found to precede the development of diverse cardiovascular diseases (CVDs). The aim of this study was to observe the protective effects of PD against H2O2-induced oxidative stress injury (OSI) in human umbilical vein endothelial cells (HUVECs) and the possible mechanism of PD in OSI treatment. HUVECs were subjected to H2O2 in the absence or presence of PD. It turned out that PD improved cell viability and adhesive and migratory abilities, inhibited the release of lactate dehydrogenase (LDH) and reactive oxygen species (ROS), and elevated the content of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD). TUNEL, fluorometric assays, and Western blotting showed that OSI upregulated the apoptosis ratio, the activity of caspase-3 and the level of proapoptotic protein Bax and decreased the level of antiapoptotic protein Bcl-2. However, PD treatment partially reversed these damage effects and Protein Kinase C (PKC) activation by thymeleatoxin (THX) in turn eliminated the antiapoptotic effect of PD. Furthermore, PD attenuated the H2O2-induced phosphorylation of PKCs α and δ and increased the phosphorylation of PKC ε. Our results indicated that PD might exert protective effects against OSI through various interactions with PKC pathway.
Highlights
Endothelial cells maintain vascular homeostasis through inhibiting platelet aggregation, preventing adhesion of leukocytes, and limiting proliferation of vascular smooth muscle and through balancing vasodilators and vasoconstrictors to manipulate vascular tone
To investigate whether PD could prevent endothelium from oxidative stress injury (OSI), human umbilical vein endothelial cells (HUVECs) were subjected to H2O2 (400 μM) in the absence or presence of PD of various concentrations (0.1–10 μg/mL) for 4 hours
The cellular adhesion rate in the H2O2 group was reduced by more than 50% compared to the control group
Summary
Endothelial cells maintain vascular homeostasis through inhibiting platelet aggregation, preventing adhesion of leukocytes, and limiting proliferation of vascular smooth muscle and through balancing vasodilators and vasoconstrictors to manipulate vascular tone. Endothelial dysfunction is reported to be the initial step of many cardiovascular pathophysiological progresses, such as hypertension [1], coronary artery disease [2], or heart failure [3]. The latest studies show that oxidative stress plays a main character in the pathogenesis of endothelial dysfunction [4], and oxidative stress induces apoptosis [5]. The PD induced antioxidative activity is reported to reverse renal injury by attenuating oxidative stress-related inflammatory responses in fructose-induced urate nephropathic [8]. PKCs are involved in the effects of PD on cardiac ischemia [14] and hypoxic pulmonary hypertension [15]. Whether PKC cellular circuit is Oxidative Medicine and Cellular Longevity involved in the prevention by PD from H2O2-induced OSI has not been elucidated to date
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