Tanshinone IIA alleviates bleomycin-induced pulmonary fibrosis by inhibiting Zbtb16

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
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Abstract

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.

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丹参酮 IIA 通过抑制 Zbtb16 减轻博莱霉素诱导的肺纤维化
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。
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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.
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