Interventional mechanism of Feibi prescription on extracellular matrix transformation in a mouse model of pulmonary fibrosis

doi:10.3969/j.issn.2095-4344.2112

Abstract

Abstract:

BACKGROUND: In the process of repair, extracellular matrix components first fill up the damaged lung tissue. However, excessive deposition of extracellular matrixes can develop pulmonary interstitial fibrosis.

OBJECTIVE: To investigate the effect of Feibi prescription on extracellular matrix transformation in mice with pulmonary fibrosis induced by bleomycin.

METHODS: Sixty male C57BL/6 mice were randomly divided into blank control group, model group, pirfenidone group, and three Feibi prescription groups (low-, middle-, and high-dose groups). There were 10 mice in each group. Except for the blank control group, the other five groups were intraperitoneally injected with bleomycin (7.5 mg/kg per day) for 10 continuous days to establish the model of pulmonary fibrosis. On day 1 after modeling, the mice in corresponding drug groups were intragastrically administered with pirfenidone (51.43 mg/kg per day) and Feibi prescription (6.43, 12.86, 25.72 mg/kg per day). Drug administration lasted for 28 days. Then, morphological changes of lung tissue in mice were observed by hematoxylin-eosin staining and Masson staining. The contents of transforming growth factor-β1 and tumor necrosis factor-α in the serum were detected by ELISA, and the expression of a-smooth muscle actin, collagen type I and collagen type III in the lung tissue was detected by western blot assay.

RESULTS AND CONCLUSION: The serum levels of transforming growth factor-β1 were significantly increased in the other groups compared with the blank control group (P < 0.01), but the levels were significantly lower in the pirfenidone, middle-dose and high-dose Feibi prescription groups than in the model group (P < 0.05, P < 0.01), and the most decline was in the high-dose Feibi prescription group. Compared with the model group, the expression of tumor necrosis factor-α was significantly reduced in the four drug groups (P < 0.01), but there was no significant difference between the drug groups (P > 0.05). Compared with the blank control group, the expression of α-smooth muscle actin was increased in the other groups to varying degrees (P < 0.05, P < 0.01). The expression of α-smooth muscle actin was significantly lower in the high-dose Feibi prescription group than the low- and middle-dose Feibi prescription groups (P < 0.05). The expression of collagen type I was significantly higher in the model and low-dose Feibi prescription groups than in the control group, whereas it was significantly lower in the middle- and high-dose Feibi prescription groups than in the model group (P < 0.05). Compared with the blank control group, the expression of collagen type III was increased to different extents in the other groups (P < 0.05, P < 0.01). Compared with the low-dose Feibi prescription group, the expression of collagen type III was significantly decreased in the middle-dose Feibi prescription group, high-dose Feibi prescription group and bleomycin group (P < 0.05, P < 0.01). To conclude, Feibi prescription can alleviate pulmonary fibrosis and inhibit the extracellular matrix transformation in bleomycin-induced pulmonary fibrosis mice. The mechanism may be related to down-regulating the levels of transforming growth factor-β1 and tumor necrosis factor-α, and inhibiting the expression of α-smooth muscle actin, collagen type I and collagen type III in the lung tissue.

Key words: Feibi prescription, pulmonary fibrosis, extracellular matrix, bleomycin, C57BL/6 mice

CLC Number:

Cheng Xue, Fang Hong, Zhang Yunke, Wu Yingen. Interventional mechanism of Feibi prescription on extracellular matrix transformation in a mouse model of pulmonary fibrosis[J]. Chinese Journal of Tissue Engineering Research, 2020, 24(31): 5038-5043.

Figures/Tables 6

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