论文部分内容阅读
[目的]研究熊果酸抑制矽肺大鼠转化生长因子β1(TGF-β1)和白介素1(IL-1)的表达及其可能作用机制。[方法]80只Wistar雄性大鼠,随机分为对照组、模型组、熊果酸组、溶剂对照组,每组20只。除对照组外,其余组采用非暴露法气管内一次性注入二氧化硅(Si O2)悬液(250 mg/kg)建立动物矽肺模型。熊果酸组自注射Si O2后每天灌胃熊果酸40 mg/kg,溶剂对照组每天灌胃质量分数为0.6%的羧甲基纤维素钠溶液(10 m L/kg),对照组灌胃生理盐水(10 m L/kg),连续56 d。ELISA法检测各组大鼠血清中IL-1和TGF-β1的质量浓度(后称“含量”),免疫组织化学法和Western blot法检测肺组织磷酸化蛋白激酶B(p-AKT1)表达情况。[结果]与对照组比较,模型组和溶剂对照组大鼠IL-1和TGF-β1含量、p-AKT1表达明显增加,差异均有统计学意义(P<0.05)。与模型组和溶剂对照组比较,熊果酸组大鼠IL-1和TGF-β1含量、p-AKT1表达下降,差异有统计学意义(P<0.05)。四组间分别进行各时间点的IL-1、TGF-β1含量与p-AKT1线性回归分析,各时间点相关系数均r>0(P<0.01)。[结论]熊果酸减少TGF-β1和IL-1表达,减缓矽肺的发展进程,其作用可能与抑制p-AKT1激活有关。
[Objective] To study the inhibitory effect of ursolic acid on the expression of transforming growth factor β1 (TGF-β1) and interleukin-1 (IL-1) in silicosis rats and its possible mechanism. [Methods] Eighty Wistar male rats were randomly divided into control group, model group, ursolic acid group and solvent control group, with 20 rats in each group. Except for the control group, the animals in the remaining groups were given a Si02 suspension (250 mg / kg) by intra-tracheal intratracheal instillation to establish the animal model of silicosis. The ursolic acid group was orally administered with ursolic acid 40 mg / kg every day after injection of Si O2, and the solvent control group was orally administered with a sodium carboxymethyl cellulose solution (10 m L / kg) at a mass fraction of 0.6% Gastric saline (10 m L / kg) for 56 days. The serum concentrations of IL-1 and TGF-β1 in rat serum were detected by ELISA. The expression of phosphorylated protein kinase B (p-AKT1) in lung tissue was detected by immunohistochemistry and Western blot. Express the situation. [Results] Compared with the control group, the levels of IL-1 and TGF-β1 and the expression of p-AKT1 in model group and solvent control group were significantly increased (P <0.05). Compared with model group and solvent control group, the content of IL-1, TGF-β1 and the expression of p-AKT1 in ursolic acid group were significantly decreased (P <0.05). The levels of IL-1, TGF-β1 and p-AKT1 at different time points were analyzed by linear regression analysis. The correlation coefficients at all time points were all higher than 0 (P <0.01). [Conclusion] UA inhibited the expression of TGF-β1 and IL-1 and slowed down the progression of silicosis, which may be related to the inhibition of p-AKT1 activation.