title: Vagal efferent fiber stimulation ameliorates pulmonary microvascular endothelial cell injury by downregulating inflammatory responses.
abstract: Electrical stimulation of the vagus nerve may have positive effects on many inflammatory diseases. This study determined the beneficial effects of vagus nerve stimulation and the mechanisms by which it attenuates lipopolysaccharide (LPS)-induced acute lung injury (ALI). Rats were intraperitoneally injected with 10 mg/kg LPS to induce ALI. The results showed that vagus nerve stimulation could improve lung injury, as evidenced by remarkable reductions in lung edema (wet-to-dry weight ratio), neutrophil infiltration (myeloperoxidase activity), and pulmonary permeability [total number of cells and protein concentrations in bronchoalveolar lavage fluid (BALF)]. In addition, vagus nerve stimulation not only decreased the expressions of Src-suppressed C kinase substrate and E-selectin proteins in lung tissue but also effectively attenuated the concentrations of the proinflammatory cytokines tumor necrosis factor-α, interleukin-1β, and interleukin-6 in BALF. These suggest that vagus nerve stimulation is a suitable treatment for LPS-induced ALI and indicate that it helps ameliorate pulmonary microvascular endothelial cell injury by downregulating inflammatory responses.
authors.affiliation: Department of Anesthesia, Critical Care Medicine & Emergency Medicine Center, Zhongnan Hospital, Wuhan University, Wuhan, 430071, Hubei Province, People's Republic of China.
authors.forename: Chao
authors.initials: C
authors.lastname: Chen
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhang
authors.forename: Zhaohui
authors.initials: Z
authors.lastname: Du
authors.forename: Min
authors.initials: M
authors.lastname: Zhang
authors.forename: Li
authors.initials: L
authors.lastname: Niu
authors.forename: Yanlin
authors.initials: Y
authors.lastname: Wang
authors.forename: Jianguo
authors.initials: J
authors.lastname: Li
mesh_terms: D054758:A Kinase Anchor Proteins / Q000096:biosynthesis; D055371:Acute Lung Injury / Q000139:chemically induced / Q000628:therapy*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D018797:Cell Cycle Proteins / Q000096:biosynthesis; D015536:Down-Regulation; D019040:E-Selectin / Q000096:biosynthesis; D042783:Endothelial Cells / Q000378:metabolism*; D007249:Inflammation / Q000378:metabolism / Q000628:therapy; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides; D008168:Lung / Q000276:immunology / Q000378:metabolism; D008297:Male; D020556:Neutrophil Infiltration / Q000276:immunology; D011654:Pulmonary Edema / Q000276:immunology / Q000628:therapy*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014630:Vagus Nerve; D055536:Vagus Nerve Stimulation
chemical_list: D054758:A Kinase Anchor Proteins; C102361:Akap12 protein, rat; D018797:Cell Cycle Proteins; D019040:E-Selectin; D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha
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