[β1 receptor blocker decreases the myocardial inflammation in the sepsis adult rats through inhibition of TLR4/NF-ΚB signaling pathway].

OBJECTIVE: To explore whether β1 receptor blocker could decrease the myocardial inflammation through the Toll-like receptor 4/nuclear factor-ΚB (TLR4/NF-ΚB) signaling pathway in the sepsis adult rats. METHODS: ) by micro pump through the caudal vein 1 hour before the CLP surgery. Samples were collected 6 hours after the modelling in each group. The average arterial pressure (MAP) and cardiac output index (CI) were monitored by PU electrical conduction ECG monitor. The levels of serum cardiac troponin I (cTnI), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) were detected by enzyme linked immunosorbent assay (ELISA). The expressions of TLR4, NF-ΚB p65, IL-1β, TNF-α in myocardial tissue was detected by Western Blot. RESULTS: : 58.6±4.3, 58.9±4.4 vs. 41.2±3.9, both P < 0.01), the levels of serum cTnI, IL-1β and TNF-α were significantly decreased [cTnI (μg/L): 1 113.81±26.64, 1 115.74±25.90 vs. 1 975.96±42.74; IL-1β (ng/L): 39.6±4.3, 38.9±4.4 vs. 61.2±3.9; TNF-α (ng/L): 43.1±2.8, 48.7±2.6 vs. 81.3±4.4, all P < 0.01], the protein expressions of myocardial tissue NF-ΚB p65, IL-1β, TNF-α were significantly decreased (NF-ΚB p65/β-actin: 0.31±0.03, 0.43±0.04 vs. 0.85±0.08; IL-1β/β-actin: 0.28±0.05, 0.32±0.03 vs. 0.71±0.06; TNF-α/β-actin: 0.18±0.04, 0.28±0.03 vs. 0.78±0.07, all P < 0.01), but there was no significant difference in protein expression of TLR4 (TLR4/β-actin: 0.89±0.07, 0.87±0.09 vs. 0.95±0.09, both P > 0.05). There was no significant difference in CI, the levels of serum cTnI, IL-1β, TNF-α, and the protein expressions of myocardial tissue TLR4, NF-ΚB p65, IL-1β, TNF-α between ES group and E5564 group (all P > 0.05). CONCLUSIONS: β1 receptor blocker esmolol may inhibit myocardial inflammatory response in sepsis adult rats through TLR4/NF-ΚB signaling pathway, thereby alleviating sepsis-induced myocardial injury.