Objective    To study the therapic effect of mA20 and its mutant mA20-ZnF4-7 plasmid on endotoxemia induced by lipopolysaccharide (LPS) in mice.      Methods    We prepared the endotoxemia animal model by assaulting mice with LPS (2.5 mg/kg). Using the method of hydrodynamics-based gene transfection

we intravenously injected mice with 10  g of plasmid DNA in 1.6 ml saline through the tail vein. The contents of TNF-α

IL-1β in blood plasma were detected by ELISA

and inflammatory reaction was also observed pathologically.      Results    The TNF-α expressions of mA20 plasmid treated group and mA20-ZnF4-7 plasmid treated group in each time point were (201.797±4.789) and (235.710±6.108) pg/ml in 6 h

(236.580±7.497) and (255.130±7.827) pg/ml in 12 h

(154.551±16.460) and (223.246±11.316) pg/ml in 24 h

which were significantly lower than those of LPS assaulting group and empty plasmid group. The IL-1β expressions of mA20 plasmid treated group and mA20-ZnF4-7plasmid treated group in each time point were (87.103±3.84) and (101.586±2.486) pg/ml in 6 h

(83.655±4.973) and (94.460±3.110) pg/ml in 12 h

(77.678±6.555) and (87.103±4.826) pg/ml in 24 h

which also significantly lower than those of LPS assaulting group and empty plasmid group. The inflammatory damage in mA20 plasmid treated group and mA20-ZnF4-7 plasmid treated group was lighter than those of LPS assaulting group and empty plasmid group

but of no significant difference in comparison with normal saline group.      Conclusion    The method of hydrodynamics-based gene transfection can efficiently deliver plasmid DNA into liver and lung. In vitro transfection of mA20-ZnF4-7 plasmid showed the similar therapeutic effect on experimental endotoxemia in mice as that of mA20 plasmid

which provides some experimental base for its clinical application.