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Protective effects of hydroxysafflower yellow A on pulmonary fibrosis in mice
浏览量 22 时间 2024-04-26 23:46:46

LUAN Zhi-hua, WEI Yan-ming, CHANG Yin-xia

Shanxi University of Chinese Medicine, Jinzhong 030619, China

Abstract: Objective: To investigate the effect of hydroxysafflower yellow A (HSYA) on pulmonary fibrosis induced by bleomycin in mice and transforming growth factor β 1(TGF-β1) /Smad signal transduction pathway regulation. Methods: The pulmonary fibrosis model was prepared by intranasal injection of bleomycin 50 μl (15 mg/kg). ICR mice were randomly divided into control group, model group, HSYA group(6 mg/kg) and dexamethasone (Dex) group(3 mg/kg), with 15 mice in each group. From the next day of modeling, HSYA and Dex groups were intraperitoneally injected with corresponding drugs, while the control group and model group were intraperitoneally injected with the same volume of normal saline, once a day, for 28 consecutive days. After 4 weeks, the mice were sacrificed and the lungs were collected. HE and Masson staining were used to observe the pathological damage of lung tissue; Immunohistochemistry, RT-qPCR and Western blot were used to detect the expressions of TGF-β1/Smad signaling pathway in lung tissues. Results: Compared with the control group, the model group showed severe alveolitis and pulmonary fibrosis. The mRNA and protein expressions of TGF-β1 and Smad3 in lung tissues were increased significantly (P<0.01), while the mRNA and protein expressions of Smad7 were decreased significantly (P<0.01). Compared with the model group, the degree of alveolitis and pulmonary fibrosis in the HSYA and Dex groups was reduced significantly. The mRNA and protein expressions of TGF-β1 and Smad3 in lung tissues of HSYA and Dex groups were decreased significantly (P<0.01), while the mRNA and protein expressions of Smad7 were increased significantly(P<0.01). Conclusion: HSYA can alleviate the pathogenesis of pulmonary fibrosis, and its mechanism may be related to the regulation of TGF-β1/Smad signaling pathway.

Key words: hydroxysafflor yellow A, pulmonary fibrosis, TGF-β1/Smad, mice    

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