Andrographolide prevented LPS-induced cardiac malfunctions in mice by inhibiting TNF-α, IL-1β, and NO production, IκB phosphorylation, and cardiac apoptosis.
Does andrographolide prevent LPS-induced cardiac malfunctions in mice?
Andrographolide shows potential as a therapeutic agent for preventing sepsis-induced myocardial malfunction by inhibiting inflammation and apoptosis in a mouse model.
BACKGROUND/AIMS: 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. CONCLUSION: 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.
Zhang et al. (Thu,) conducted a other in LPS-induced cardiac malfunction. Andrographolide was evaluated on Cardiac malfunctions, TNF-α, IL-1β, NO production, IκB phosphorylation, and cardiac apoptosis. Andrographolide prevented LPS-induced cardiac malfunctions in mice by inhibiting TNF-α, IL-1β, and NO production, IκB phosphorylation, and cardiac apoptosis.
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