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虎杖苷通过抑制炎症和上皮-间质转化、抑制TGF-β/Smad信号通路来改善肺纤维化。

Polydatin ameliorates pulmonary fibrosis by suppressing inflammation and the epithelial mesenchymal transition inhibiting the TGF-β/Smad signaling pathway.

作者信息

Qiu Yue, Pan Xue, Hu Yahui

机构信息

Department of Chinese Medicine, The Third Affiliated Hospital of Beijing University of Chinese Medicine No. 51, Xiaoguan Street, Chaoyang District Beijing 100029 China

Department of Chinese Medicine, Beijing University of Chinese Medicine Beijing 100029 China.

出版信息

RSC Adv. 2019 Mar 12;9(14):8104-8112. doi: 10.1039/c8ra08659a. eCollection 2019 Mar 6.

DOI:10.1039/c8ra08659a
PMID:35521205
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9061874/
Abstract

Pulmonary fibrosis is a chronic and progressive lung disease which results in a loss of pulmonary function and eventually respiratory failure. Inflammation and epithelial mesenchymal transition (EMT) play important roles in the pathogenesis of pulmonary fibrosis. This study aimed to investigate the therapeutic effect of polydatin (PD) in bleomycin-induced pulmonary fibrosis. A bleomycin-induced pulmonary fibrosis animal model used SD rats. Morphological changes were analyzed by hematoxylin-eosin staining. RT-qPCR and western blot were used for the detection of the expression of TGF-β1, collagen I, collagen III, E-cadherin, fibronectin and the ratios of p-Smad2/Smad2, p-Smad3/Smad3. The concentrations of PICP, PIIINP, TNF-α, IL-1β, IL-6 and IL-17 were measured by enzyme linked immunosorbent assay (Elisa) assay. Results showed that PD attenuated bleomycin-induced pulmonary fibrosis. The beneficial effect of PD was possibly related to the inhibition of inflammation and EMT through suppressing the TGF-β/Smad signaling pathway. Our findings suggested that PD might be a potential therapeutic candidate in the treatment of pulmonary fibrosis.

摘要

肺纤维化是一种慢性进行性肺部疾病,会导致肺功能丧失并最终引发呼吸衰竭。炎症和上皮-间质转化(EMT)在肺纤维化的发病机制中起重要作用。本研究旨在探讨虎杖苷(PD)对博来霉素诱导的肺纤维化的治疗效果。采用博来霉素诱导的肺纤维化动物模型,选用SD大鼠。通过苏木精-伊红染色分析形态学变化。采用RT-qPCR和蛋白质印迹法检测转化生长因子-β1(TGF-β1)、Ⅰ型胶原、Ⅲ型胶原、E-钙黏蛋白、纤连蛋白的表达以及p-Smad2/Smad2、p-Smad3/Smad3的比值。采用酶联免疫吸附测定(ELISA)法检测血清Ⅲ型前胶原N端肽(PICP)、Ⅲ型前胶原肽(PIIINP)、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和白细胞介素-17(IL-17)的浓度。结果表明,PD减轻了博来霉素诱导的肺纤维化。PD的有益作用可能与通过抑制TGF-β/Smad信号通路来抑制炎症和EMT有关。我们的研究结果表明,PD可能是治疗肺纤维化的潜在候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4159/9061874/7be80bfadfb7/c8ra08659a-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4159/9061874/fcdca373f94d/c8ra08659a-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4159/9061874/315c442bfb2f/c8ra08659a-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4159/9061874/cc56729e5121/c8ra08659a-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4159/9061874/7be80bfadfb7/c8ra08659a-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4159/9061874/fcdca373f94d/c8ra08659a-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4159/9061874/315c442bfb2f/c8ra08659a-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4159/9061874/cc56729e5121/c8ra08659a-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4159/9061874/7be80bfadfb7/c8ra08659a-f4.jpg

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