姜黄素对肺纤维化大鼠肺组织TGF—β1与HGF表达的影响

Curcumin affects expression of HGF and TGF-β1 of lung tissue in pulmonary fibrosis

目的探讨TGF—β1与HGF在肺纤维化中的作用及不同浓度姜黄素对博莱霉素诱导的肺纤维化大鼠肺组织中HGF及TGF—β1表达的影响。方法健康雄性SD大鼠90只，随机分为6组。分别为空白对照组（A组）、模型组（B组）、泼尼松治疗组（C组）、姜黄素50组（D组）、姜黄素100组（E组）、姜黄素200组（F组），应用气管内给予博莱霉素制作肺纤维化动物模型。造模7、14、28d时分三次取材。用RT-PCR，Western blot检测各组肺组织中HGF及TGF—β1 mRNA及蛋白的表达。结果A组28dTGF—β1的光密度值（0．693±0．028）及灰度值（0．96±0．10）最低。B组28dTGF—β1光密度值（1．586±0．020）及灰度值（1．77±0．15）最高、F组28dTGF—β1光密度值（0．881±0．032）及灰度值（1．19±0．12）与B组比较最低。而HGF的光密度值及灰度值的检测正好相反。F组28dHGF的光密度值及灰度值最高。B组与D组的HGF和TGF—β1光密度值及灰度值差异无统计学意义（P〉0．05）。结论姜黄素抑制肺纤维化的机制之一可通过增高HGF的活性同时减低TGF—β1的活性来实现，这种作用有一定的剂量依赖性。

Objective To explore the effect of Curcumin on TGF-β1 and HGF in pulmonary fibrosis and the effect of different concentrations of Curcumin on the expression of HGF and TGF-β1 in pulmonary fibrosis. Methods 90 health male SD rats were randomly divided into six groups as follows： the control group （group A） , model group （group B） , prednisolone-treated group （group C ）, and groups of low （D group）, middle（ group E） and high（ group F） dose curcumin （50, 100, and 200 mg/kg, respectively）. Animal model of pulmonary fibrosis was produced in SD rats by the endotracheal bleomyeiu, samples were obtained on days 7, 14, and 28. The expression of HGF and TGF-β1 were measured by RT-PCR and Western blot. Results The light density values （0. 693 ± 0. 028） and gray value （0. 96 ± 0. 10 ） of TGF-β1 on day 28 of group A was the lowest, while the light density values （1. 586 ±0. 020） and gray value （ 1.77 ± 0. 15）of group B was the highest, the light density values （0. 881 ±0. 032） and gray value （ 1. 19 ±0. 12） of group F was lower than group B. But the light density value and gray value of HGF showed reverse, the light density values and gray value of HGF on day 28 of group F was the highest, there was no statistical difference between group B and group D （ P 〉 0. 05）. Conclusions The protective effect of Cucumin against pulmonary fibrosis may be through stimulating the activity of HGF and inhibiting the activity of TGF- β1 in a dose-dependent manner.