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目的以内毒素攻击模型观察腹腔转染炎症诱导启动子ＳＡＡ３指导的ＨＩＬ１０基因在小鼠体内表达的可行性及对炎症介质表达的影响。方法小鼠分３组，采用腹腔注射法转染脂质体／ＤＮＡ复合物，４８小时后ＬＰＳ攻击，测定不同时间ＨＩＬ１０的诱导表达（ＲＴ－ＰＣＲ、ＥＬＩＳＡ）及分布（免疫组化），不同时间ＴＮＦ－α、ＩＬ－６表达测定（ＥＬＩＳＡ法）。结果ＲＴ－ＰＣＲ证明ＬＰＳ攻击后基因转染小鼠肝脏ＨＩＬ１０表达迅速增加（１２．６～１４．９倍），维持１～５天；免疫组化显示肝细胞及ｋｕｐｆｅｒ细胞有强阳性反应细胞。ＨＩＬ１０基因转染显著下调肝脏ＴＮＦ－α（６６．２１％～４４．８％）及ＩＬ－６表达（４２．２５％）（Ｐ＜０．０５），显著降低血清ＴＮＦ－α（３３．６％～５３．６％）及ＩＬ－６（１６％～４０％）水平（Ｐ＜０．０５）。结论ＰＳＡＡ３ＨＩＬ１０诱导表达体系腹腔转染可被炎症诱导，迅速启动并在小鼠肝脏表达，白细胞介素１０（ＩＬ－１０）基因转染显著抑制肝脏ＴＮＦ－α、ＩＬ－６表达，显著降低血清炎症介质的水平。
OBJECTIVE: To investigate the feasibility of intraperitoneal transfection of inflammation-inducible promoter SAA3-directed HIL10 gene in mice and the effect on the expression of inflammatory mediators. Methods The mice were divided into three groups. The liposome / DNA complexes were transfected by intraperitoneal injection. After 48 hours, the mice were challenged by LPS. The expression of HIL10 at different time (RT-PCR, ELISA) and distribution (immunohistochemistry) Time TNF-α, IL-6 expression (ELISA method). Results RT-PCR showed that the expression of HIL10 in the liver of mice transfected with LPS increased rapidly from 12.6 to 14.9 folds and maintained for 1 to 5 days. Immunohistochemistry showed strong positive cells in hepatocytes and kupfer cells. HIL10 gene transfection significantly decreased the levels of TNF-α (66.21% -44.8%) and IL-6 (42.25%) in liver (P <0.05) % ~ 53.6%) and IL-6 (16% -40%) (P <0.05). Conclusion Intraperitoneal transfection of PSAA3HIL10-induced expression system can be induced by inflammation and promptly activated and expressed in mouse liver. Interleukin-10 gene transfection significantly inhibits the expression of TNF-α and IL-6 in the liver and significantly reduces serum inflammation Medium level.