Recent Advances in Studies of Molecular Hydrogen against Sepsis

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Recent Advances in Studies of Molecular Hydrogen against Sepsis ( recent-advances-studies-molecular-hydrogen-against-sepsis )

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Int. J. Biol. Sci. 2019, Vol. 15 1262 Figure 1. Molecular hydrogen exerts biological effects. Molecular hydrogen can be ingested in a variety of ways and exerts biological effects, including anti-oxidation, anti-inflammation, anti-apoptosis, anti-shock, and autophagy regulation through scavenging free radicals directly and regulating signal transduction and gene expression indirectly. Based on these therapeutic advantages, molecular hydrogen has been widely used in studies of organ protection during sepsis in recent years, and has yielded ideal results. Molecular hydrogen attenuates the injury and dysfunction of important organs (heart, liver, lung, kidneys, and brain) and physiological barriers (epithelial cell barrier, vascular endothelial cell barrier) by suppressing oxidative stress and inflammation as well as reducing apoptosis [6-10] and regulating sepsis-induced autophagy[11, 12]. However, the underlying molecular mechanisms of these effects have not been elucidated. Therefore, understanding the research status of molecular hydrogen against sepsis and the underlying mechan- isms are of great significance for treating sepsis. Molecular hydrogen against organ injury induced by sepsis Lipopolysaccharide (LPS) is a component of the cell wall of Gram-negative bacteria and the most important pathogenic factor in sepsis. It has been demonstrated that molecular hydrogen extenuates LPS-induced ALI in rats by reducing the release of inflammatory factors, inhibiting the aggregation of inflammatory cells, reducing oxidative stress and apoptosis[8, 11, 13]. Moreover, molecular hydrogen alleviates pulmonary edema caused by LPS through upregulating the expression of pulmonary aquaporin (AQP)[14]. These lung protective effects are thought to be associated with a reduction in LPS-induced p38 mitogen-activated protein kinase (p38 MAPK) and c-Jun N-terminal kinase (JNK) activation by molecular hydrogen[11, 14, 15]. In addition to protecting the mature lung, HRS also alleviates bronchopulmonary dysplasia (BPD) induced by LPS in neonatal mice[16]. Fibroblast growth factor receptor 4 (FGFR4) and vascular endothelial growth factor receptor 2 (VEGFR2) are important for maintaining alveolar structures and lung development[17, 18]. Oral intake of HRS ameliorates LPS-induced suppression of genes encoding FGFR4, VEGFR2, and heme oxygenase 1 (HO-1) in neonatal mice[16]. In addition, study showed[19] that LPS promotes the alveolar epithelial-mesenchymal transition (EMT) and pulmonary fibrosis by increasing the production of reactive oxygen species (ROS) and transforming growth factor-β (TGF-β). HRS alleviates oxidative stress and pulmonary fibrosis by reducing LPS-induced E-cadherin loss and α-smooth muscle actin production[20]. The liver is the most important organ for removing cytotoxic substances from the body, but may become overloaded by sepsis and exhibit injury and dysfunction[6]. A series of studies have reported thatHRSreducesliverdamagecausedbyendotoxin in rats [6, 21, 22]. Iketani et al. found that HRS Alleviates liver injury induced by oxidative stress through further increasing LPS-induced HO-1 expression and decreasing endothelin-1 (ET-1) expression [6]. Xu et al. demonstrated that HRS mitigates the pathological injury of the septic rat liver and improves survival rate by reducing the release of inflammatory cytokines and reducing hepatocyte apoptosis and oxidative stress[22]. Inhibiting signal- ing pathways, such as p38 MAPK, JNK, extracellular regulated protein kinase (ERK), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and reducing the second mitochondria- derived activator of caspase (Smac) level contribute to HRS-mediated liver protection[22]. Multiple studies[23-25] have demonstrated that HRS protects renal function by reducing serum creatinine and urea nitrogen levels and relieving renal structural damage caused by sepsis. Liu et al. reported that inhaling molecular hydrogen alleviates brain damage and cognitive dysfunction in septic rats by inhibiting the neuronal inflammatory response and oxidative stress, while neuronal apoptosis is reduced by increasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and HO-1[26]. In the septic pancreatitis rat model, Zhang et al. found that HRS exerts anti-inflammation, anti-oxidant, and antibacterial effects by inhibiting the NF-κB signaling pathway[27]. It has been demonstrated that http://www.ijbs.com

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