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Objective To investigate the antagonistic effect and mechnism of the effect of cyprohe ptadine (Cyp) on endotoxic shock in rats. Methods Endotoxic shock was produced in rats by iv injection of lipopolysaccharides (LPS) (5?mg/kg). Tumor necrosis fator (TNF_α) mRNA expression was assessed by Northern blot. Plasma TNF_α content was measured by radioimmunoassay. P lasma superoxide dismutase (SOD) activity and malondialdehyde (MDA) content wer e measured. The intracellular free calcium concentration (_i) in single endothelial cells was determined by laser scanning confocal microscop y (LSCM). Results Cyp 5?mg/kg injected immediately after iv LPS raised the mean arterial blood p ressure (MABP) of shocked rats and improved their 24?h survival rate. Meanwhil e, Cyp markedly decreased TNF_α mRNA levels in rat liver (18±10 vs LPS+sal ine 38±10, P <0.01) as well as plasma TNF_α content [(7.8±2.4) μg/L vs LPS+saline (21.5±3.2) μg/L, P <0.01)]. It enhanced plasma SOD act ivity [(1037.2±112.8) NU/L vs LPS+saline (615.4±92.6) NU/L, P <0.01] , reduced the MDA content [(5.2±1.1) μmol/L vs LPS+saline (9.8±1.5) μmol/L, P <0.01], and inhibited TNF_α-induced _i eleva tion. Conclusion Cyp exerts an anti-endotoxic shock effect by inhibiting TNF_α gene expression , enhancing SOD activity, reducing lipid peroxidation, and preventing [Ca 2+ ]_i overload.
Objective To investigate the antagonistic effect and mechnism of the effect of cyprohe ptadine (Cyp) on endotoxic shock in rats. Methods Endotoxic shock was produced in rats by iv injection of lipopolysaccharides (LPS) (5? Mg / kg). Tumor necrosis fator ( TNF_α) mRNA expression was assessed by Northern blot. Plasma TNF_α content was measured by radioimmunoassay. P lasma superoxide dismutase (SOD) activity and malondialdehyde (MDA) content wer e measured. by laser scanning confocal microscop y (LSCM). Results Cyp 5? mg / kg injected immediately after iv LPS raised the mean arterial blood ressure (MABP) of shocked rats and improved their 24? h survival rate. Meanwhil e, Cyp markedly decreased TNFα mRNA levels in rat liver (18 ± 10 vs LPS + saline 38 ± 10, P <0.01) , P <0.01)]. It enhanced plasma SOD act ivity [(1037.2 The MDA content [(5.2 ± 1.1) μmol / L vs. LPS + saline (9.8 ± 1.5) μmol / L, P <0.01] P <0.01], and inhibited TNF_α-induced_i eleva tion. Conclusion Cyp exerts an anti-endotoxic shock effect by inhibiting TNFα gene expression, enhancing SOD activity, reducing lipid peroxidation, and preventing [Ca 2+] _i overload.