The changes of HMGB-1 in patients with sepsis and the effect of carbachol on prevention of HMGB-1 / 中国综合临床

ABSTRACT

Objective To observe the changes of HMGB-1 of burned patient with sepsis and to investigate the effect of carbaehol on production of HMGB-1 from human monocytes stimulated by lipopolysaccharide(LPS) and its mechanism. Methods The peripheral blood samples of burned patients with sepsis and healthy donors were taken for isolation of monoeyte. The subjects were divided into six groups the menocytes group were added only with 1640 culture medium,LPS group were added only with LPS;nicotine group and carbachol group were with carbachol first or nicotine for 5 rain and then with LPS. The levels of HMGB-1 were tested by EIJSA. α-bungarotoxin + carba-chol group were added with atropine or α-bungarotoxin for 5 min and then were given carbachol and 5 min later were stimulated with LPS. 48 h-incubation later supemate were collected for the detection of HMGB-1 by ELISA. Results HMGB-1 levels of burned patients with sepsis were ( 12.94±6.54)μ/L,which were much higher than that of healthy donors( [ (2.01±0.03 )μ/L), P <0.01 ]. When monoeytes were stimulated by LPS alone, concentrations of HMGB-1 were (9.39±1.37 ) μ/L, which were obviously higher than that of controls [( 1.48±0.69 ) μ/L), P < 0.01]. Mter pretreated by carbaehol or nicotine,concentrations of HMGB-1 were (3.52±1.64)μ/L and (4.01± 1.56) μ/L respectively, which were obviously decreased compared with that of LPS stimulation alone group ( P < 0.01). When pretreatedby atropine before addition of carbachol, there was no significant changes in concentrations of HMGB-1 [ (3.87±2.01 )μ/L]. When pretreated with α-Bungaretoxin before carbachol adminitration, inhibitive effect of carbachol on production of HMGB-1 were blocked [(8.97±1.97 )μ/L ]. Conclusion The release of HMGB-1 in burned patients with sepsis is increased. Carbachol could obviously reduce the production of HMGB-1, which may affect through activating α 7 subunit of cholinergic N receptor.