title: Andrographolide Attenuates LPS-Induced Cardiac Malfunctions Through Inhibition of IκB Phosphorylation and Apoptosis in Mice.
abstract: OBJECTIVE
  Cardiac malfunction is a common complication in sepsis and significantly increases the mortality of patients in septic shock. However, no studies have examined whether andrographolide (And) reduces LPS-induced myocardial malfunction.
  
  
  METHODS
  Left ventricular systolic and diastolic functions were examined using echocardiography. TNF-α and IL-1β protein levels were detected by an enzyme-linked immunosorbent assay (ELISA). NO oxidation products were determined using Griess reagent. Protein expression levels of inhibitors of NF-κBα (IκB) and phospho-IκB were determined via Western blot. Oxidative injury was determined by measuring myocardial lipid peroxidation and superoxide dismutase activity. Cardiac apoptosis was examined by terminal deoxynucleotidyl transferase-mediated dUTP nickend-labeling (TUNEL) and cardiac caspase 3/7 activity.
  
  
  RESULTS
  And blunted LPS-induced myocardial malfunctions in mice. LPS induced TNF-α, IL-1β, and NO production as well as I-κB phosphorylation. Cardiac apoptosis was attenuated via incubation with And, but the extent of oxidative injury remained unaffected.
  
  
  CONCLUSIONS
  And prevents LPS-induced cardiac malfunctions in mice by inhibiting TNF-α, IL-1β, and NO production, IκB phosphorylation, and cardiac apoptosis, indicating that And may be a potential agent for preventing myocardial malfunction during sepsis.
authors.forename: Jinlong
authors.initials: J
authors.lastname: Zhang
authors.forename: Didi
authors.initials: D
authors.lastname: Zhu
authors.forename: Yulin
authors.initials: Y
authors.lastname: Wang
authors.forename: Yunfeng
authors.initials: Y
authors.lastname: Ju
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D053179:Caspase 7 / Q000378:metabolism; D004224:Diterpenes / Q000494:pharmacology*; D004452:Echocardiography; D006321:Heart / Q000187:drug effects*; D020672:I-kappa B Proteins / Q000378:metabolism*; D053583:Interleukin-1beta / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009206:Myocardium / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D004224:Diterpenes; D020672:I-kappa B Proteins; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; C030419:andrographolide; D013482:Superoxide Dismutase; D053148:Caspase 3; D053179:Caspase 7