title: Paeoniflorin improves survival in LPS-challenged mice through the suppression of TNF-α and IL-1β release and augmentation of IL-10 production.
abstract: Lipopolysaccharide (LPS) plays an important role in Gram-negative bacteria-induced sepsis and multiple organ dysfunction syndrome, which are still the leading cause of high mortality in intensive care units. Although paeoniflorin (Pae) has reportedly exhibited anti-inflammatory effect and protection against immunological liver injury in mice, it is not known whether Pae improve survival in endotoxemic mice. The purpose of this study was to determine the effect of Pae on the mortality, multiple organ dysfunction and cytokine production in lipopolysaccharide (LPS)-treated mice. We found that pretreatment with Pae decreased mortality, reduced lung and kidney injury, decreased serum creatinine level and improve systolic function of heart in mice challenged with LPS. Further experiments showed that Pae inhibited LPS-stimulated tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) release and promoted LPS-induced interleukin-10 (IL-10) production. Our results indicate that Pae protects mice against lethal LPS challenge, at least in part, through inhibiting TNF-α and IL-1β production and accelerating IL-10 expression.
authors.affiliation: Department of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou 510632, Guangdong, China.
authors.forename: Wenjuan
authors.initials: W
authors.lastname: Cao
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Jingjing
authors.initials: J
authors.lastname: Liu
authors.forename: Yuan
authors.initials: Y
authors.lastname: Wang
authors.forename: Xuemei
authors.initials: X
authors.lastname: Peng
authors.forename: Daxiang
authors.initials: D
authors.lastname: Lu
authors.forename: Renbin
authors.initials: R
authors.lastname: Qi
authors.forename: Yanping
authors.initials: Y
authors.lastname: Wang
authors.forename: Huadong
authors.initials: H
authors.lastname: Wang
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000627:therapeutic use*; D001565:Benzoates / Q000008:administration & dosage / Q000627:therapeutic use*; D001952:Bridged-Ring Compounds / Q000008:administration & dosage / Q000627:therapeutic use*; D016207:Cytokines / Q000032:analysis / Q000097:blood*; D004452:Echocardiography; D005960:Glucosides / Q000008:administration & dosage / Q000627:therapeutic use*; D006321:Heart / Q000187:drug effects; D016753:Interleukin-10 / Q000097:blood; D053583:Interleukin-1beta / Q000097:blood; D007668:Kidney / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D007677:Kidney Function Tests; D008070:Lipopolysaccharides / Q000633:toxicity*; D008099:Liver / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D008111:Liver Function Tests; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D039821:Monoterpenes; D009206:Myocardium / Q000276:immunology / Q000473:pathology; D011654:Pulmonary Edema / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D016019:Survival Analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D006027:Glycosides
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D001565:Benzoates; D001952:Bridged-Ring Compounds; D016207:Cytokines; D005960:Glucosides; D016753:Interleukin-10; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D039821:Monoterpenes; D014409:Tumor Necrosis Factor-alpha; C482199:lipopolysaccharide, E coli O55-B5; C015423:peoniflorin; D006027:Glycosides