stilbenes and Hyperoxia

To explore the effect of resveratrol on the levels of sirtuin 1 (SIRT1) and reactive oxygen species (ROS) in peripheral blood mononuclear cells (PBMCs) of premature infants exposed to hyperoxia.. Peripheral blood and isolated PBMCs from premature infants (gestational age<32 weeks) without oxygen supplement were collected and were randomly assigned into four groups: control, air+resveratrol, hyperoxia, and hyperoxia+resveratrol. The PBMCs were cultured in vitro for 48 hours, then the ROS content in PBMCs was measured by laser scanning confocal microscopy. Malondialdehyde (MDA) content in the medium was measured by the whole spectrum spectrophotometer. SIRT1 positioning was assessed by immunofluorescence. SIRT1 expression levels in PBMCs were measured by Western bolt.. Compared with the control group, the level of SIRT1 in the air+resveratrol group increased significantly (P<0.05). The levels of ROS and MDA and the SIRT1 transposition rate in the hyperoxia group increased significantly, while the expression level of SIRT1 decreased significantly compared with the control group (P<0.05). The levels of ROS and MDA and the SIRT1 transposition rate decreased significantly (P<0.05), and the expression level of SIRT1 increased significantly in the hyperoxia+resveratrol group (P<0.05).. Resveratrol can increase SIRT1 expression in PBMCs and inhibit SIRT1 shuttle from nucleus to cytoplasm in order to increase the ability of antioxidative stress in premature infants exposed to hyperoxia, thereby reducing the oxidative stress injury in premature infants.

Topics: Female; Humans; Hyperoxia; Infant, Newborn; Infant, Premature; Leukocytes, Mononuclear; Lipid Peroxidation; Male; Oxidative Stress; Resveratrol; Sirtuin 1; Stilbenes

By assessing silent mating-type information regulation 2 homolog 1 (SIRT1) nucleocytoplasmic shuttling and reactive oxygen species (ROS) levels in peripheral blood mononuclear cells (PBMCs), this study aimed to explore the role of SIRT1 in premature infants after exposure to hyperoxia and assess the protective effects of resveratrol (Res).. Firstly, ROS levels as well as SIRT1 translocation and expression in PBMCs samples were evaluated from 40 premature infants with different oxygen amounts received at birth. Then, PBMCs, from additional 40 premature infants administered no oxygen at birth, were used to establish an in vitro model of hyperoxia.. In infants that received O. Res inhibits ROS release in PBMCs from preterm infants exposed to hyperoxia, likely by preventing SIRT1 nucleocytoplasmic shuttling and increasing SIRT1 expression.

Topics: Active Transport, Cell Nucleus; Cells, Cultured; Female; Humans; Hyperoxia; Infant, Newborn; Infant, Premature; Leukocytes, Mononuclear; Malondialdehyde; Oxygen; Reactive Oxygen Species; Resveratrol; Sirtuin 1; Stilbenes

Bronchopulmonary dysplasia (BPD) is a chronic lung disease that causes significant morbidity and mortality in premature infants. Inflammation and oxidative injury play an important role in the pathogenesis of BPD. Resveratrol is an antioxidant and anti-inflammatory agent. In this study, the histopathological and biochemical effects of resveratrol on a hyperoxia-induced lung injury model in newborn rats were investigated.. The experiment was performed on newborn rat pups from the 3(rd) to 13(th) postnatal day and they were randomly divided into four groups: Group 1 (air-exposed + saline, n = 10), Group 2 (air-exposed + resveratrol, n = 11), Group 3 (hyperoxia-exposed + saline, n = 6) and Group 4 (hyperoxia-exposed + resveratrol, n = 7). Resveratrol was administered (30 mg/kg/day) intraperitoneally. The histopathological effects of resveratrol on lung tissue were assessed by alveolar surface area, fibrosis, and smooth muscle actin (SMA) score, and the biochemical effects on lung tissue were assessed by glutathione (GSH), superoxide dismutase (SOD), nitric oxide (NO), tumor necrosis factor-α (TNF-α), and nuclear factor kappa B (NF-κB) levels.. The alveolar surface area, fibrosis, SMA score, and NO levels were found to be significantly higher in Group 3 compared with Group 1 (p < 0.05). In addition, it was found that resveratrol treatment significantly reduced the SMA score and the NO and TNF-α levels, and increased the GSH and SOD levels in the hyperoxia group (p < 0.05).. This experimental study showed that oxidative stress and NO contributed to the pathogenesis of hyperoxia-induced lung injury, and that resveratrol had a preventive effect on hyperoxic lung injury through its anti-inflammatory and antioxidant properties.

Topics: Animals; Animals, Newborn; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Bronchopulmonary Dysplasia; Disease Models, Animal; Humans; Hyperoxia; Infant, Newborn; Infant, Premature; Lung; Lung Injury; Rats, Wistar; Resveratrol; Stilbenes

Topics: Animals; Animals, Newborn; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Bronchopulmonary Dysplasia; Disease Models, Animal; Humans; Hyperoxia; Lung Injury; Rats; Resveratrol; Stilbenes

There is many evidence that inhalation of high oxygen concentration has a toxic influence on pulmonary function and structures. Hyperoxia-induced oxidative stress is well characterized in rodents and has been used as a valuable model of human respiratory distress syndrome. We have previously shown that hyperoxic exposure of guinea pigs is associated with suppression of cough reflex. The goal of this study was to determine the effects of dietary intake of antioxidant flavonoids (Flavin7, Vita Crystal Slovakia Ltd., 2 ml/kg b.w.) on hyperoxia-induced oxidative stress in lung tissue directed on cough reflex. The experimental group (n = 8) was pretreated with Flavin7 as a single daily dose for 14 days and subsequently exposed to 100% 02 for 60 h. Hyperoxic group (n = 8) inhaled 100% Oz only. Control group (n = 8) was exposed to normoxia. Cough was induced by inhalation of citric acid aerosol at time before and after exposure to hyperoxia. Cough was also induced by mechanical stimulation of airways in anaesthetized animals just after the end of oxygen exposition. When to compare animal groups before and after hyperoxia, our results have shown a significant decrease 2 (1-6) vs 6 (4-6) p = 0.041 in citric acid-induced cough in hyperoxic animals and no significant changes 8 (5.5-8.5) vs 5 (4-6.5) p = 0.055 in animals with antioxidant therapy. Mechanically-induced cough after hyperoxia was not influenced by substitution with flavonoids. In conclusion, our results indicate that flavonoids attenuated hyperoxia-induced down-regulation especially of chemically-induced cough (Tab. 2, Fig. 2, Ref. 30). Full Text (Free, PDF) www.bmj.sk.

Topics: Animals; Antioxidants; Citric Acid; Cough; Flavonoids; Guinea Pigs; Hyperoxia; Male; Oxidative Stress; Resveratrol; Stilbenes