stilbenes and Respiratory-Distress-Syndrome

The putative cardiovascular risks and benefits of the ingestion of wine and alcohol-containing spirits have been well publicized; however, less attention has been focused upon the health effects of wine and spirits consumption on the respiratory system. This paper will highlight epidemiologic, clinical and experimental data on the effects of wine and distilled spirits [and the chemical components thereof] on lung function, chronic obstructive pulmonary disease progression, lung cancer risk, risk of developing acute respiratory distress syndrome, high altitude pulmonary edema and wine [sulfite] associated asthma. Several studies have demonstrated a positive [beneficial] effect of light-to-moderate wine consumption on pulmonary function, while chronic ingestion of distilled spirits may have either no effect, or a negative effect. Studies in Scandinavia, Europe and South America have suggested a possible protective effect of wine ingestion against lung cancer, especially adenocarcinoma. Resveratrol [3,5,4'-trihydroxystilbene] a polyphenolic compound found in red wine, has anti-oxidant, anti-inflammatory and estrogen agonist effects and may be responsible for some of the health benefits of wine. The spectrum of potentially beneficial clinical effects of resveratrol and other wine-derived compounds is discussed.

Topics: Adenocarcinoma; Alcohol Drinking; Alcoholic Beverages; Alcoholism; Altitude Sickness; Antioxidants; Asthma; Female; Humans; Lung; Lung Neoplasms; Male; Pulmonary Disease, Chronic Obstructive; Pulmonary Edema; Respiratory Distress Syndrome; Resveratrol; Stilbenes; Sulfites; Wine

Topics: Adult; Aged; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Cytarabine; Diphosphates; Drug Resistance, Neoplasm; Drug Synergism; Feasibility Studies; Female; Fibrin Fibrinogen Degradation Products; Hemorrhage; Humans; Leukemia, Myeloid, Acute; Male; Middle Aged; Myelodysplastic Syndromes; Prodrugs; Respiratory Distress Syndrome; Salvage Therapy; Stilbenes; Treatment Outcome; Young Adult

Mitophagy removes dysfunctional mitochondria and is known to play an important role in the pathogenesis of several diseases; however, the role of mitophagy in acute respiratory distress syndrome (ARDS) remains poorly understood. While we have previously demonstrated that polydatin (PD) improves lipopolysaccharide (LPS)-induced ARDS, the specific mechanism remains unclear. In present study, we aimed to determine whether PD activates Parkin-dependent mitophagy to protect against LPS-induced mitochondria-dependent apoptosis and lung injury. To establish the ARDS model, C57BL/6 mice were intratracheally injected with LPS (5 mg/kg) in vivo and Beas-2B cells were exposured to 0.5 mM LPS in vitro. Our results indicate that PD facilitates Parkin translocation to mitochondria and promotes mitophagy in ARDS-challenged mice and LPS-treated Beas-2B cells. However, PD-induced mitophagy was suppressed in Parkin-/- mice and Parkin siRNA transfected cells, indicating that PD activates Parkin-dependent mitophagy. Furthermore, the protective effects of PD against LPS-induced mitochondria-dependent apoptosis and lung injury were suppressed when Parkin was depleted both in vivo and in vitro. The inhibition of mitophagy with mitophagy inhibitor mitochondrial division inhibitor-1 in vivo and silencing of autophagy-related gene 7 in vitro also blocked the protective effects mediated by PD. Our data suggest that Parkin-dependent mitophagy induced by PD provides protection against mitochondria-dependent apoptosis in ARDS.

Topics: Animals; Apoptosis; Drug Evaluation, Preclinical; Drugs, Chinese Herbal; Fallopia japonica; Glucosides; Male; Mice, Inbred C57BL; Mitophagy; Phytotherapy; Respiratory Distress Syndrome; Stilbenes; Ubiquitin-Protein Ligases

The aim of the present research was to investigate the protecting effects of 3,5,4'-tri-O-acetylresveratrol (AC-Rsv) on LPS-induced acute respiratory distress syndrome (ARDS). Lung injuries have been evaluated by histological examination, wet-to-dry weight ratios, and cell count and protein content in bronchoalveolar lavage fluid. Inflammation was assessed by MPO activities and cytokine secretion in lungs and cells. The results showed that AC-Rsv significantly reduced the mortality of mice stimulated with LPS. Pretreatment of AC-Rsv attenuated LPS-induced histological changes, alleviated pulmonary edema, reduced blood vascular leakage, and inhibited the MPO activities in lungs. What was more, AC-Rsv and Rsv treatment reduced the secretion of TNF-α, IL-6, and IL-1β in lungs and NR8383 cells, respectively. Further exploration revealed that AC-Rsv and Rsv treatment relieved LPS-induced inhibition on SIRT1 expression and restrained the activation effects of LPS on MAPKs and NF-κB activation both in vitro and in vivo. More importantly, in vivo results have also demonstrated that the protecting effects of Rsv on LPS-induced inflammation would be neutralized when SIRT1 was in-hibited by EX527. Taken together, these results indicated that AC-Rsv protected lung tissue against LPS-induced ARDS by attenuating inflammation via p38 MAPK/SIRT1 pathway.

Topics: Acetates; Animals; Capillary Permeability; Cells, Cultured; Inflammation Mediators; Lipopolysaccharides; Lung; Male; MAP Kinase Signaling System; Mice; Respiratory Distress Syndrome; Resveratrol; Sirtuin 1; Stilbenes

The effects of polydatin on endotoxin-induced acute lung injury were studied in rats. The lung injury was induced by infusion of inactivated E. coli 30 min after MPS blockade with red cell membrane. It was found that pretreatment with polydatin resulted in marked reduction of lung wet-to-dry weight ratio, lung permeability index (LPI), neutrophil count in BALF and hemoconcentration. The elevation of lung tissue MDA and the decrease in plasma GSH-Px activity were greatly improved with polydatin. There was significant correlation between LPI and lung MDA level (r = 0.741, P < 0.01). Postmortem examination revealed that polydatin attenuated the histopathological changes. We conclude that polydatin protectsral against endotoxin-induced acute lung injury.

Topics: Animals; Drugs, Chinese Herbal; Endotoxins; Escherichia coli; Female; Glucosides; Lung; Male; Rats; Rats, Sprague-Dawley; Respiratory Distress Syndrome; Stilbenes