| Objective 1 Discussing the distribution regularity of TCM syndrome of the patients with idiopathic pulmonary fibrosis(IPF). 2 Discussing the influence of SQCC capsule to the alveolar epithelial mesenchymal transformation(EMT) on pulmonary fibrosis of tats induced by bleomycin(BLM). 3 Discussing the Wnt/β-catenin signal path’s possible role in the process of EMT.Methods 1Clinical observation: A TCM syndrome’s questionnaire was made after rewiewing the related literatures to gather the general information(including sex, age, couse of disease, smoking history and complications) and four diagnosis of TCM of 76 patients. The distribution regularity of TCM syndrome of the patients with IPF was got by statistical analysis. 2 Animal experiments: The 128 male SD rats were randomly divided into four groups, including blank group, model group, SQCC group and prednisone group. Each group has 32 rats. The three groups of rats were made PF model by dropping BLM into trachea after adaptive feeding 7 days. The blank group of rats were dropped the same amount of normal saline. The medicine was given by gavage 1 day later. The blank group was given the same amount of normal saline. Rats were sacrificed on the 7th, 14 th, 21 th and 28 th day after gavage. We dissected the lung for pathological observation by HE staining and collagen deposition by Masson staining. The expressions of E-Cad, α-SMA and Vimentin were analyzed by immunohistochemical and the gene expressions of Wnt1, Wnt2 and β-catenin mRNA were detected by RT-PCR.Results 1 Clinical observation : The top five syndromes were syndrome of Qi-Yin deficiency with blood-stasis(13.16%), syndrome of phlegm-heat obstructing lung(10.53%), syndrome of phlegm and blood stasis obstructing lung(9.21%), syndrome of Qi deficiency of lung and kidney(7.89%) and syndrome of deficiency of both Qi and Yin of lung(7.89%). 2 Animal experiments: 2.1 HE-staining: The alveolar structures of blank group rats were mainly clear and complete. The alveolar structures of model group rats were in disorder. The alveolar cavity collapsed most and there were inflammatory cells on it.The alveolar septum began to thicken on the 7th day. The alveolar cavities were full of inflammatory cells and the alveolar septum continued to be thickened. The proliferation of fibroblasts made the formation of fibrous tissue and collagen deposition on the 14 th day. The inflammatory cells were less than before on the 14 th day.The organization structure began to repair and the alveolar septum further broadened. There were no inflammatory cells and a large number of hyperplasia of fibroblasts and fibrous tissues formed on the 28 th day. The above pathological changes had varying degrees of ease on the SQCC group and prednisone group compared with model group corresponding time point respectively. The SQCC group and prednisone group were close to the degree. 2.2 Masson staining: There were only small distributions of blue collagen fibers on the alveolar septum on the blank group. There were blue collagen fibers depositions, which focused primarily on terminal bronchial wall, vessel wall and alveolar septum on the model group on the 7th day. The blue color of each part deepened and the collagen fibers deposited further on the 14 th day. The blue area increased and the color was deeper on the 21 th and 28 th day, which showed that a large amount of collagen deposited and diffuse fibrous tissue formed. The above pathological changes had varying degrees of ease on the SQCC group and prednisone group compared with model group corresponding time point respectively. The SQCC group and prednisone group were close to the degree. 2.3 E-cad, α-SMA and Vimentin protein: Compared with the blank group, the expression of E-cad protein in the model group was significantly lower(P<0.05), and it was significantly lower than the SQCC group and prednisone group on the 7th, 14 th, 21 th and 28 th day(P<0.05). Compared with the blank group, the expressions of α-SMA and Vimentin protein in the model group were significantly higher(P<0.05), and it were significantly higher than the SQCC group and prednisone group on the 7th, 14 th, 21 th and 28 th day(P<0.05). The differents of E-cad and Vimentin between SQCC group and prednisone group were not statistically significant the same four time points(P(29)0.05). The different of α-SMA between SQCC group and prednisone group was not statistically significant on the 7th, 14 th and 21 th day(P(29)0.05). But on the 28 th day, the expression in the SQCC group was significantly lower than prednisone group(P(27)0.05).The expressions of E-cad, α-SMA and Vimentin protein in the blank group were not statistically significant(P(29)0.05) but E-cad significantly decreased gradually and α-SMA and Vimentin significantly increased gradually in the model group、SQCC group and prednisone group on the 14 th, 21 th and 28 th day(P<0.05). 2.4 Wnt1, Wnt2 and β-catenin mRNA: Compared with the blank group, the expressions of Wnt1, Wnt2 and β-catenin mRNA in the model group were significantly higher(P<0.05), and they were significantly higher than the SQCC group and prednisone group on the 7th, 14 th, 21 th and 28 th day(P<0.05). The differents between SQCC group and prednisone group were not statistically significant the same four time points(P(29)0.05).The expressions of the three mRNA in the blank group were not statistically significant the same four time points(P(29)0.05), but increased at first and then decreased in model group. The highest was on the 21 th day and the differences were statistically significant(P<0.05).The expressions of the Wnt1 and Wnt2 mRNA were statistically significant and the β-catenin mRNA was not in the SQCC group and prednisone group on the14 th, 21 th and 28 th day.Conclusion 1Syndrome of Qi-Yin deficiency with blood-stasis is the common and main syndrome. 2 SQCC capsule can inhibit the inflammation of lung and collagen deposition of the rats with PF. It can inhibit PF partly by increasing the expression of E-cad protein and decreasing the the expression of α-SMA and Vimentin protein. 3 SQCC capsule can inhibit the expressions of Wnt1, Wnt2 and β-catenin mRNA. So we guess that SQCC capsule can inhibit PF from progressing by means of influencing on related links of Wnt/β-catenin signaling system. |
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