丹参酮 IIA 通过抑制 Zbtb16 减轻博莱霉素诱导的肺纤维化

IF 3.3 3区 医学 Q2 PHARMACOLOGY & PHARMACY Pulmonary pharmacology & therapeutics Pub Date : 2024-01-06 DOI:10.1016/j.pupt.2024.102285
Huijuan Zhang, Jianli Qiu, Qianyi Zhao, Yong Zhang, Haitao Zheng, Ziying Dou, Yongbin Yan
{"title":"丹参酮 IIA 通过抑制 Zbtb16 减轻博莱霉素诱导的肺纤维化","authors":"Huijuan Zhang,&nbsp;Jianli Qiu,&nbsp;Qianyi Zhao,&nbsp;Yong Zhang,&nbsp;Haitao Zheng,&nbsp;Ziying Dou,&nbsp;Yongbin Yan","doi":"10.1016/j.pupt.2024.102285","DOIUrl":null,"url":null,"abstract":"<div><p><span>Pulmonary fibrosis<span><span><span> is a complex disease that can occur in a variety of clinical settings. The Zinc Finger<span> and BTB Domain Containing 16 (Zbtb16) is a transcription factor and has not been studied in pulmonary fibrosis. Lung tissues from rats which were treated with </span></span>bleomycin and </span>Tanshinone IIA<span><span><span> (Tan IIA) were collected for mRNA sequencing. Zbtb16, a differentially expressed gene, was screened. Using adeno-associated virus to knock down Zbtb16 in rats, it was found that the lung index and the content of hydroxyproline in lung tissue were decreased. HE and Masson staining revealed that pathological symptoms of lung </span>histopathology<span> were relieved after Zbtb16 knockdown. Protein expressions of α-SMA, Collagen I and </span></span>Fibronectin were significantly decreased after Zbtb16 knockdown </span></span></span><em>in vivo</em> and <em>in vitro</em><span>. Meanwhile, the protein content of TGF-β1 and the phosphorylation of Smad2/3 were inhibited by Zbtb16 knockdown. Conversely, under the treatment<span> of Tan IIA and TGF-β1, overexpression of Zbtb16 improved cell viability, increased the expression of fibrosis-related proteins, and promoted the phosphorylation of Smad 2/3. All above demonstrates that Zbtb16 inhibition ameliorates pulmonary fibrosis and suppresses the TGF-β/Smad pathway. Furthermore, Zbtb16 mediates the inhibitory process of Tan IIA on pulmonary fibrosis. This study provides a novel candidate therapeutic target for pulmonary fibrosis.</span></span></p></div>","PeriodicalId":20799,"journal":{"name":"Pulmonary pharmacology & therapeutics","volume":null,"pages":null},"PeriodicalIF":3.3000,"publicationDate":"2024-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Tanshinone IIA alleviates bleomycin-induced pulmonary fibrosis by inhibiting Zbtb16\",\"authors\":\"Huijuan Zhang,&nbsp;Jianli Qiu,&nbsp;Qianyi Zhao,&nbsp;Yong Zhang,&nbsp;Haitao Zheng,&nbsp;Ziying Dou,&nbsp;Yongbin Yan\",\"doi\":\"10.1016/j.pupt.2024.102285\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p><span>Pulmonary fibrosis<span><span><span> is a complex disease that can occur in a variety of clinical settings. The Zinc Finger<span> and BTB Domain Containing 16 (Zbtb16) is a transcription factor and has not been studied in pulmonary fibrosis. Lung tissues from rats which were treated with </span></span>bleomycin and </span>Tanshinone IIA<span><span><span> (Tan IIA) were collected for mRNA sequencing. Zbtb16, a differentially expressed gene, was screened. Using adeno-associated virus to knock down Zbtb16 in rats, it was found that the lung index and the content of hydroxyproline in lung tissue were decreased. HE and Masson staining revealed that pathological symptoms of lung </span>histopathology<span> were relieved after Zbtb16 knockdown. Protein expressions of α-SMA, Collagen I and </span></span>Fibronectin were significantly decreased after Zbtb16 knockdown </span></span></span><em>in vivo</em> and <em>in vitro</em><span>. Meanwhile, the protein content of TGF-β1 and the phosphorylation of Smad2/3 were inhibited by Zbtb16 knockdown. Conversely, under the treatment<span> of Tan IIA and TGF-β1, overexpression of Zbtb16 improved cell viability, increased the expression of fibrosis-related proteins, and promoted the phosphorylation of Smad 2/3. All above demonstrates that Zbtb16 inhibition ameliorates pulmonary fibrosis and suppresses the TGF-β/Smad pathway. Furthermore, Zbtb16 mediates the inhibitory process of Tan IIA on pulmonary fibrosis. This study provides a novel candidate therapeutic target for pulmonary fibrosis.</span></span></p></div>\",\"PeriodicalId\":20799,\"journal\":{\"name\":\"Pulmonary pharmacology & therapeutics\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":3.3000,\"publicationDate\":\"2024-01-06\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Pulmonary pharmacology & therapeutics\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1094553924000014\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"PHARMACOLOGY & PHARMACY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pulmonary pharmacology & therapeutics","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1094553924000014","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}
引用次数: 0

摘要

肺纤维化是一种复杂的疾病,可发生在各种临床环境中。锌指和含BTB域16(Zbtb16)是一种转录因子,但尚未对其在肺纤维化中的作用进行过研究。研究人员收集了接受博莱霉素和丹参酮 IIA(Tan IIA)治疗的大鼠肺组织,并对其进行了 mRNA 测序。对差异表达基因 Zbtb16 进行了筛选。利用腺相关病毒敲除大鼠的 Zbtb16,发现肺指数和肺组织中羟脯氨酸的含量均有所下降。HE 和 Masson 染色显示,Zbtb16 基因敲除后,肺组织病理学症状得到缓解。体内和体外敲除 Zbtb16 后,α-SMA、胶原蛋白 I 和纤连蛋白的蛋白表达量均显著下降。同时,Zbtb16敲除后,TGF-β1的蛋白含量和Smad2/3的磷酸化均受到抑制。相反,在 Tan IIA 和 TGF-β1 的处理下,过表达 Zbtb16 可提高细胞活力,增加纤维化相关蛋白的表达,促进 Smad 2/3 的磷酸化。所有这些都表明,抑制 Zbtb16 可改善肺纤维化并抑制 TGF-β/Smad 通路。此外,Zbtb16 还介导了 Tan IIA 对肺纤维化的抑制过程。这项研究为肺纤维化提供了一个新的候选治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Tanshinone IIA alleviates bleomycin-induced pulmonary fibrosis by inhibiting Zbtb16

Pulmonary fibrosis is a complex disease that can occur in a variety of clinical settings. The Zinc Finger and BTB Domain Containing 16 (Zbtb16) is a transcription factor and has not been studied in pulmonary fibrosis. Lung tissues from rats which were treated with bleomycin and Tanshinone IIA (Tan IIA) were collected for mRNA sequencing. Zbtb16, a differentially expressed gene, was screened. Using adeno-associated virus to knock down Zbtb16 in rats, it was found that the lung index and the content of hydroxyproline in lung tissue were decreased. HE and Masson staining revealed that pathological symptoms of lung histopathology were relieved after Zbtb16 knockdown. Protein expressions of α-SMA, Collagen I and Fibronectin were significantly decreased after Zbtb16 knockdown in vivo and in vitro. Meanwhile, the protein content of TGF-β1 and the phosphorylation of Smad2/3 were inhibited by Zbtb16 knockdown. Conversely, under the treatment of Tan IIA and TGF-β1, overexpression of Zbtb16 improved cell viability, increased the expression of fibrosis-related proteins, and promoted the phosphorylation of Smad 2/3. All above demonstrates that Zbtb16 inhibition ameliorates pulmonary fibrosis and suppresses the TGF-β/Smad pathway. Furthermore, Zbtb16 mediates the inhibitory process of Tan IIA on pulmonary fibrosis. This study provides a novel candidate therapeutic target for pulmonary fibrosis.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
CiteScore
6.20
自引率
0.00%
发文量
41
审稿时长
42 days
期刊介绍: Pulmonary Pharmacology and Therapeutics (formerly Pulmonary Pharmacology) is concerned with lung pharmacology from molecular to clinical aspects. The subject matter encompasses the major diseases of the lung including asthma, cystic fibrosis, pulmonary circulation, ARDS, carcinoma, bronchitis, emphysema and drug delivery. Laboratory and clinical research on man and animals will be considered including studies related to chemotherapy of cancer, tuberculosis and infection. In addition to original research papers the journal will include review articles and book reviews. Research Areas Include: • All major diseases of the lung • Physiology • Pathology • Drug delivery • Metabolism • Pulmonary Toxicology.
期刊最新文献
Hyperbaric oxygen therapy as an immunomodulatory intervention in COVID-19-induced ARDS: Exploring clinical outcomes and transcriptomic signatures in a randomised controlled trial Interaction between fluticasone furoate and umeclidinium in passively sensitized isolated human airways Chest CT assess the impact of omalizumab treatment on airway remodeling in refractory asthma Elexacaftor/tezacaftor/ivacaftor, a game-changer in cystic fibrosis: The Portuguese experience Editorial Board
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1