补肾通络方抑制肺纤维化及对相关细胞因子含量的影响

Inhibition of bushen tongluo formula on pulmonary fibrosis and the effect on the relevant cytokines

目的从调节细胞因子含量的角度来探讨补肾通络方对抑制肺纤维化的作用机制。方法采用博来霉素诱导建立实验性肺纤维化大鼠模型,以氢化可的松琥珀酸钠为对照,观察补肾通络方对肺纤维化大鼠肺组织病理形态、血清羟脯氨酸(HYP)、透明质酸(HA)、层粘连蛋白(LN)及肺组织白介素(IL)-1、IL-6、肿瘤坏死因子(TNF)-α含量的影响。结果与正常组比较,模型组大鼠肺组织病理纤维化显著,炎性反应明显,同时伴有血清HYP、HA、LN升高(P<0.05,P<0.01),肺组织IL-1、IL-6、TNF-α含量升高(P<0.05,P<0.01)。与模型组相比,补肾通络高剂量组大鼠血清HYP、HA、LN含量明显下降(P<0.05);补肾通络低剂量组LN含量明显下降(P<0.01),氢化可的松琥珀酸钠对照组HYP、HA、LN含量明显下降(P<0.05,P<0.01),补肾通络高剂量组和氢化可的松琥珀酸钠对照组大鼠IL-1、IL-6、TNF-α含量明显下降(P<0.05,P<0.01),肺组织病理形态的改善。结论补肾通络方可通过调节实验性肺纤维化大鼠肺组织炎性细胞因子含量,抑制肺纤维化。

Objective To explore the effect mechanism of bushen tongluo formula on pulmonary fibrosis in view of the regulation of cytokine content.Methods The rate model of experimental pulmonary fibrosis was induced by bleomycin.Taking hydrocortisone sodium succinate as the control,the effect of bushen tongluo formula was observed on the pathological morphology of lung tissue and the expressions of hydroxyproline(HYP),hyaluronic acid(HA),laminin(LN),lnterleukin(IL)-1,IL-6 and tumor necrosis factor(TNF)-αin serum in the rats with pulmonary fibrosis.Results Compared with the normal group,in the model group,the pathological fibrosis of rat lung tissue was significant,the inflammatory reaction was obvious and the levels of serum HYP,HA and LN were increased(P<0.05,P<0.01)and the levels of IL-1,IL-6 and TNF-αin lung tissue were increased(P<0.05,P<0.01).Compared with the model group,in the high-dose bushen tongluo formula group,the levels of serum HYP,HA and LN were reduced obviously(P<0.05).LN was reduced obviously in the low-dose bushen tongluo group(P<0.01).In the control group of hydrocortisone sodium succinate,the levels of HYP,HA and LN were reduced obviously(P<0.05 or P<0.01).In the high-dose bushen tongluo formula group and the control group,the levels of IL-1,IL-6 and TNF-αwere reduced obviously(P<0.01,P<0.01).The pathological morphology of lung tissue was relieved.Conclusion Bushen tongluo formula inhibits pulmonary fibrosis through regulating the content of inflammatory cytokines of lung tissue in the rats with experimental pulmonary fibrosis.