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利用刀豆蛋白A（ConA）诱发实验性小鼠肝损伤模型，研究假密环菌杂多糖Y－HW和活性蛋白对ConA诱导小鼠肿瘤坏死因子a（TNF-a）和γ-干扰素（IFN－γ）蛋白产物表达的影响。结果表明，ConA组血浆TNF－a产物含量为（15．15±1．34）×10-4mg／ml，IFN－γ为（7．155±1．43）×10－4mg／ml。而多糖组血浆TNF－a产物含量为（4．024±0．31）×10-4mg／ml，活性蛋白组为（4．934±0．45）×10－mg／ml，与ConA组比较有极显著性差异P＜0·001，多糖组IFN－γ为（5．622±1．01）×10－4mg／ml，活性蛋白组为（3．624±0．56）×10-4mg／ml，与ConA组比较P＜0．001，与正常对照组比较P＜0．05。实验结果显示：（1）假密环菌杂多糖Y－HW和活性蛋白能降低由ConA引起的实验性小鼠TNF－a蛋白产物的表达；（2）杂多糖与ConA一样可增加IFN－γ蛋白产物的表达，但活性蛋白却不能。
The experimental mice liver injury model was induced by concanavalin A (ConA), and the effect of Y-HW and active protein of pseudoguannavirus on tumor necrosis factor a (TNF-α) and interferon-γ IFN-γ) protein product expression. The results showed that the content of plasma TNF-a in ConA group was (15.15 ± 1.34) × 10-4mg / ml and IFN-γ was (7.155 ± 1.43) × 10-4mg / ml. However, the content of plasma TNF-a in the polysaccharide group was (4.024 ± 0.31) × 10-4mg / ml and the active protein group was (4.934 ± 0.45) × 10-mg / ml, which was significantly lower than that in the ConA group (P <0.001), polysaccharide group (5.622 ± 1.01) × 10-4mg / ml and active protein group (3.624 ± 0.56) × 10-4mg / Ml, compared with ConA group P <0.001, compared with the normal control group P <0.05. The experimental results showed that: (1) Y-HW and active protein of Pseudomonas aeruginosa could reduce the expression of TNF-a protein in experimental mice induced by ConA; (2) Heteropolysaccharide could increase IFN-γ like ConA Protein product expression, but active protein can not.