9:20 AM - 9:30 AM
[O2-E-AM1-03] The chronic administration of Porphylomonas gingivals -LPS effects cardiac dysfunction by activating beta-adrenergic receptors signaling.
Keywords:交感神経系、内毒素(LPS)、筋小胞体
Periodontitis was recently demonstrated to induce activation of sympathetic nerve activity and thus cardiovascular disease might be susceptible in periodontitis patients from clinical studies. However, the mechanism has not been clearly understood. The aim of the present study was to investigate the effects of lipopolysaccharide derived from Porphyromonas gingivalis (PG-LPS) at a dose equivalent to the circulating levels in periodontitis patients on cardiac function in mice, together with the underlying mechanisms. Mice were divided into 4groups:1) Control, 2) PG-LPS (0.8mg/kg/day ip for 7 days), 3) non-selective β-blocker propranolol, (PPL) (via the drinking water containing 1g/L), and 4) PG LPS+PPL. We first examined cardiac function by echocardiography and found that cardiac function was significantly decreased by the treatment of PG-LPS, but propranolol ameliorated the dysfunction. Cardiac fibrosis (Masson-trichrome staining) and myocyte apoptosis (TUNEL staining) were significantly increased by the treatment of PG-LPS, but propranolol blocked these changes. The PG-LPS-induced cardiac dysfunction was associated with increased phospholamban phosphorylation at threonine-17 , as well as ryanodine receptor 2 phosphorylation at serine-2814. Importantly, propranolol again blocked both phosphorylations. These data suggest that chronic PG-LPS infusion might affect cardiac dysfunction via activation of the sympathetic nervous system.