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机构地区:[1]天津医科大学,300232
出 处:《天津医药》2001年第3期165-167,I003,I004,共5页Tianjin Medical Journal
摘 要:目的:探讨肿瘤坏死因子(TNF-α)在内毒素(LPS)所致急性肺损伤(ALI)发病过程中的作用,及神农33(SN 33)注射液对TNF-α基因表达的影响。方法:给大鼠静脉注射LPS,建立ALI模型。分别采用ELISA和Northern blotting方法检测LPS攻击后不同时间血清中TNF-α含量,及肺组织TNF-α mRNA水平的变化。同时以地塞米松(DXM)为对照,观察神农33注射液对TNF-α释放和表达的影响,及肺病理形态学的变化。结果:LPS诱发大鼠ALI过程中血清TNF-α水平均高于正常对照组(P<0.01)。肺组织TNF-α mRNA表达明显增高,以神农33保护的大鼠其TNF-α含量和mRNA表达均低于相应时相LPS攻击组,且肺损伤程度减轻。结论:TNF-α在LPS诱导的ALI过程中起着重要作用,神农33注射液可以抑制TNF-α的释放和表达,对肺脏有一定保护作用。To investigate the effect of Shen Nong 33(SN 33)(a traditional Chinese medicine)on gene expression of tumor necrosis factor(TNF-a)in lipopolysacchride(LPS)-induced acute lung injury(ALI)rat. Methods:The levels of TNF-a in rat serum were measured with ELISA and TNF-a gene expression in rat lung tissue was observed with Northern Blotting at different time courses. The effects of SN 33 and DXM on release and gene expression of TNF-a and the changes of lung his-topathology were observed at the same time. Results:The serum levels of TNF-a rapidly increased after LPS injection. TNF-a gene expression in rat lung tissue was dramatically upregulated during ALL Both SN 33 and DXM could decreased the serum levels and lung gene expression of TNF-a. Conclusion: TNF-a plays an essential role in an inflammatory response. LPS-induced ALI may be prevented by SN 33 and DXM.
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