[Protective effects of hydroxysafflower yellow A on pulmonary fibrosis in mice].

Zhi-Hua Luan, Yan-Ming Wei, Yin-Xia Chang
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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.

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[羟基红花黄A对小鼠肺纤维化的保护作用]。
目的:探讨羟基花黄A (HSYA)对博来霉素致小鼠肺纤维化的影响及转化生长因子β1 (TGF-β1) /Smad信号转导通路的调节作用。方法:鼻腔注射博来霉素50 μl (15 mg/kg)制备肺纤维化模型。将ICR小鼠随机分为对照组、模型组、HSYA组(6 mg/kg)和地塞米松组(3 mg/kg),每组15只。从造模第二天起,HSYA组和Dex组大鼠腹腔注射相应药物,对照组和模型组大鼠腹腔注射等量生理盐水,每天1次,连续28 d。4周后处死小鼠,取肺。采用HE、Masson染色观察肺组织病理损伤;采用免疫组织化学、RT-qPCR和Western blot检测肺组织中TGF-β1/Smad信号通路的表达。结果:与对照组比较,模型组大鼠出现严重的肺泡炎和肺纤维化。肺组织中TGF-β1、Smad3 mRNA和蛋白表达量显著升高(P<0.01), Smad7 mRNA和蛋白表达量显著降低(P<0.01)。与模型组比较,HSYA组和Dex组大鼠肺泡炎和肺纤维化程度均明显减轻。HSYA组和Dex组肺组织中TGF-β1、Smad3 mRNA和蛋白表达量均显著降低(P<0.01), Smad7 mRNA和蛋白表达量均显著升高(P<0.01)。结论:HSYA可缓解肺纤维化的发病机制,其机制可能与调控TGF-β1/Smad信号通路有关。
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CiteScore
0.70
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发文量
53
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