Browsing by Subject "Sulfur dioxide"

Now showing 1 - 7 of 7
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    Effect of endogenous sulfur dioxide in regulating cardiovascular oxidative stress
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Zhu, Mingzhu; Du, Junbao; Liu, Angie Dong; Holmberg, Lukas; Tang, Chaoshu; Jin, Hongfang
    In the middle of the 1980s, nitric oxide received extensive attention because of its significant effects in life science. Then, carbon monoxide and hydrogen sulfide were discovered to be gasotransmitters playing important roles in regulating cellular homeostasis. As a common air pollutant, sulfur dioxide (SO2) can cause great harm to the human body by producing free radicals, which causes oxidative damage to various organs. Recently, endogenous SO2 was found to be produced in the cardiovascular system and might be a bioactive molecule regulating the physiological activities including cardiovascular oxidative stress.
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    Effect of sulfur dioxide on vascular biology
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Cai, Huijun; Wang, Xinbao
    Gasotransmitters, such as nitric oxide, carbon monoxide and hydrogen sulfide, can be generated endogenously. These gasotransmitters play important roles in vascular biology, including vasorelaxation and inhibition of vascular smooth muscle cell (VSMC) proliferation. In recent years, sulfur dioxide (SO2) has been considered as the fourth gasotransmitter. SO2 is present in air pollution. Moreover, SO2 toxicity, including oxidative stress and DNA damage, has been extensively reported in previous studies. Recent studies have shown that SO2 can be endogenously generated in various organs and vascular tissues, where it regulates vascular tone, vascular smooth cell proliferation and collagen synthesis. SO2 can decrease blood pressure in rats, inhibit smooth muscle cell proliferation and collagen accumulation and promote collagen degradation, and improve vascular remodelling. SO2 can decrease cardiovascular atherosclerotic plaques by enhancing the antioxidant effect and upregulating nitric oxide/nitric oxide synthase and hydrogen sulfide/ cystathionine-γ-lyase pathways. SO2 can also ameliorate vascular calcification via the transforming growth factor - β1/Smad pathway. The effect of SO2 on vascular regulation has attracted great interest. SO2 may be a novel mediator in vascular biology
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    Potential therapeutic effect of SO2 on fibrosis.
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2019) Wang, Xin Bao; Cui, Hong; Du, Jun Bao
    Fibrosis is a pathological feature of most chronic diseases and leads to the dysfunction of various organs. However, there is currently no effective method for treating fibrosis. In recent years, a small gas, sulfur dioxide (SO2), which can be generated endogenously in mammals, has been found to have vasorelaxation activity, improve cardiac function and decrease myocardial injury. Endogenous SO 2 also mediates the process of fibrosis. Inhibition of endogenous SO 2 can aggravate small pulmonary artery remodeling and abnormal collagen accumulation. SO 2 treatment significantly improves pulmonary fibrosis and pulmonary arterial remodeling. Overexpression of the key enzymes associated with endogenous SO 2 generation, aspartate aminotransferase (AAT) 1 and AAT2, mimics the effect of SO 2 on the down-regulation of collagen synthesis, while AAT1 or AAT2 knockdown aggravates abnormal collagen accumulation in vascular smooth muscle cells (VSMCs). SO 2 also improves myocardial fibrosis induced by myocardial infarction or diabetes in rats, and inhibits myocardial fibroblast proliferation and migration by the extracellular signal- regulated protein kinase pathway. The mechanisms underlying the inhibition of fibrosis by SO 2 are related to its antioxidant effect, anti-inflammation effect, improvement in cardiac function, and cell proliferation inhibition. Therefore, SO 2 has a potential therapeutic effect on fibrosis.
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    Sulfur dioxide ameliorates rat myocardial fibrosis by inhibiting endoplasmic reticulum stress
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Wang, Xin Bao; Cui, Hong; Du, Jun Bao
    Myocardial remodeling occurs after myocardial infarction (MI), the leading cause of mortality worldwide. Although myocardial fibrosis plays an important role in the process of myocardial remodeling, there is not yet an effective method of reducing it. The aim of the present study was to determine the effects of sulfur dioxide (SO2) on myocardial fibrosis and the possible mechanisms of these effects. SO2 treatment reduced the extent of myocardial fibrosis and post-MI levels of collagens I and III in the left-ventricular myocardium. SO2 also improved MI-induced thinning of the left ventricular wall while enlarging the left ventricular internal diameter. SO2 was able to reduce matrix metalloproteinase (MMP)-9 activity and increase tissue matrix metalloproteinase inhibitor (TIMP)-1 content in myocardium after MI. However, the mechanism underlying these effects of SO2 on myocardial fibrosis are unknown. Western blot analysis of endoplasmic reticulum (ER) stress-related proteins showed that glucose-regulated protein 78, C/EBP homologous protein, caspase-12, and phosphorylated eukaryotic initiation factor 2α expression levels were significantly increased in MI rats and decreased by SO2 treatment. The ER stress promoter dithiothreitol reversed these effects of SO2. In conclusion, SO2 alleviated myocardial fibrosis in MI rats through a mechanism related to inhibition of excessive ER stress.
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    Sulfur dioxide restores calcium homeostasis disturbance in rat with isoproterenol-induced myocardial injury
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2012) Chen, Shanshan; Du, Junbao; Liang, Yingfang; Zhang, Rongyuan; Tang, Chaoshu; Jin, Hongfang
    Backgrounds: sulfur dioxide (SO2) could relieve isoproterenol (ISO)-induced myocardial injury, while the mechanism is unclear. This study aims to explore whether the protective effect of SO2 on ISO-induced myocardial injury was mediated by the restoration of calcium homeostasis disturbance in cardiomyocyte. Methods and results: Rats were randomly divided into four groups: ISO group, ISO+SO2 group, control group and SO2 group. Content of Ca2+ in H9c2 cells was assayed using confocal microscope, and cardiac function parameters were measured by echocardiography. Plasma biochemical values and myocardial ultra-structure changes were measured. Meanwhile, the activity, protein and gene levels of sarcoplasmic reticulum Ca2+ ATPase (SERCA), and protein and phosphorylation of phospholamban (PLN) were detected. We found SO2 derivatives could restore the decreased cardiac function, the abnormal lactate dehydrogenase, creatine kinase, alpha-hydroxybutyrate dehydrogenase, potassium, calcium, blood urea nitrogen and the damaged myocardial ultra-structure in rats, and regulate the increased Ca2+ content in H9c2 induced by ISO. In addition, compared with ISO group, the decreased activities, protein and mRNA level of SERCA, as well as the decreased protein phosphorylation level of PLN in myocardial tissues were increased in ISO+SO2 group. Conclusion: SO2 derivatives might relieve calcium overload in association with the upregulating expression of SERCA and p-PLN/PLN by myocardial tissues in rats with ISO-induced myocardial injury
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    Sulfur dioxide: a physiologic endothelium-derived relaxing factor
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Wang, Xin Bao; Cui, Hong; Du, Jun Bao
    The gasotransmitter nitric oxide was classified as the first endothelium-derived relaxant factor, and opened a new era in cardiovascular research. Another small gas, sulfur dioxide (SO2), can also be generated endogenously in mammals. Recent studies have shown that SO2 may play important roles in the cardiovascular system. At low concentrations, the vasodilatory effect of SO2 is endothelium-dependent. The vasodilation induced by an endothelium-derived relaxant factor is achieved by the opening of potassium channels, and hyperpolarization of the membranes of vascular smooth muscle cells. This feature is in accordance with that of SO2. The vasodilatory effect of SO2 is related to the opening of adenosine triphosphatesensitive potassium channels and high-conductance calcium-activated potassium channels. The 3'-5'-cyclic guanosine monophosphate pathway and activation of nitric oxide synthase are also involved in the endothelium-derived relaxant factor effect of SO2. The vasodilatory effect of gaseous SO2 is much stronger than that of its derivatives (bisulfite and sulfite). It is suggested that SO2 may be a candidate endotheliumderived relaxant factor, which could lead to a new era of research into cardiovascular disease in mammals.
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    Sulfur dioxide: foe or friend for life?
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Wang, Xin Bao; Cui, Hong; Liu, Xiao Hong; Du, Jun Bao
    Sulfur dioxide (SO2) is a toxic gas and air pollutant. The toxic effects of SO2 have been extensively studied. Oxidative damage due to SO2 can occur in multiple organs. Inhaled SO2 can also cause chromosomal aberrations, DNA damage and gene mutations in mammals. However, SO2 can also be generated from the sulfur-containing amino acid, Lcysteine. Recent studies have shown that SO2 has a vasorelaxant effect, and ameliorates pulmonary hypertension and vascular remodeling. SO2 can also reduce lung injury and myocardial injury in rats. In addition, SO2 reduces myocardial ischemia-reperfusion injury and atherosclerotic lesions. Therefore, SO2 exerts both detrimental and protective effects in mammals. Is SO2 a foe or friend for life?