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太光平 汪仕良 王 裴 陈 渝 刘 昕 王桂珍 章 波 黎 鳌
【摘要】 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kupffer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 PSAA3 HIL10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。
【关键词】 白细胞介素10 基因疗法 白细胞介素6 肿瘤坏死因子α 内毒素血症
Inhibition of IL-10 Gene Transfection on TNF-α、IL-6 Production in Endotoxemia Mouse
TAI Guangping, WANG Shiliang, LI Ao, et al.
Burn Research Institute of PLA, Southwestern Hospital, Third Military Medical University, Chongqing 400038
【Abstract】 Objective To investigate the possibility of HIL-10 gene expression and its inhibitory effects of inflammation on TNF-α and IL-6 production in endotoxemia mouse model. Methods Experimental mice were divided into three groups. Each mouse was administered PSAA3 HIL-10 intraperitoneally and then challenged with LPS. HIL-10 expression was detected by RT-PCR, ELISA and immunohistochemistry at indicated time. TNF-α and IL-6 were determined by ELISA method. Results HIL-10 expression was rapidly increased by 12.6-14.9 fold after LPS challenge and maintained 1-5 days. Positive cell of HIL-10 expression was mainly found in Kupffer cell and hepatocyte. HIL-10 gene transfection significantly decreased not only the expression of hepatic TNF-α (66.21%-44.8％) and IL-6 (42.25％) (P<0.05), but also the serum levels of TNF-α (33.6%-53.6％) and IL-6 (16%-40％)(P<0.05). Conclusions The expression of PSAA3 HIL-10 in the liver of transfected mouse can be induced by inflammation and in an inflammation inducible pattern. HIL-10 can markedly inhibit endotoxin-induced hepati[1] [2] 下一页
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