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In vivo, in vitro, and in silico approaches in the detailed study of di-butyl phthalate (DBP), a plasticizer-induced lung fibrosis via Nrf-2/Keap-1/HO-1 pathway and its regulation.通过Nrf-2/Keap-1/HO-1途径及其调控机制,采用体内、体外和计算机模拟方法详细研究邻苯二甲酸二丁酯(DBP)这种增塑剂诱导的肺纤维化。
Bioorg Chem. 2025 Jan;154:107970. doi: 10.1016/j.bioorg.2024.107970. Epub 2024 Nov 22.
2
Understanding the molecular basis of anti-fibrotic potential of intranasal curcumin and its association with mitochondrial homeostasis in silica-exposed mice.了解鼻内姜黄素抗纤维化潜力的分子基础及其与暴露于二氧化硅的小鼠中线粒体动态平衡的关系。
Mitochondrion. 2024 Sep;78:101943. doi: 10.1016/j.mito.2024.101943. Epub 2024 Aug 8.
3
Repeated Silica exposures lead to Silicosis severity via PINK1/PARKIN mediated mitochondrial dysfunction in mice model.反复的二氧化硅暴露通过 PINK1/PARKIN 介导的线粒体功能障碍导致小鼠模型中矽肺的严重程度。
Cell Signal. 2024 Sep;121:111272. doi: 10.1016/j.cellsig.2024.111272. Epub 2024 Jun 27.
4
Naringenin attenuated airway cilia structural and functional injury induced by cigarette smoke extract via IL-17 and cAMP pathways.柚皮素通过白细胞介素-17和环磷酸腺苷途径减轻香烟烟雾提取物诱导的气道纤毛结构和功能损伤。
Phytomedicine. 2024 Apr;126:155053. doi: 10.1016/j.phymed.2023.155053. Epub 2023 Sep 2.
5
Cilia-related diseases.纤毛相关疾病。
J Cell Mol Med. 2023 Dec;27(24):3974-3979. doi: 10.1111/jcmm.17990. Epub 2023 Oct 13.
6
Mechanisms of airway epithelial injury and abnormal repair in asthma and COPD.哮喘和 COPD 中气道上皮损伤和异常修复的机制。
Front Immunol. 2023 Jul 13;14:1201658. doi: 10.3389/fimmu.2023.1201658. eCollection 2023.
7
Seriously cilia: A tiny organelle illuminates evolution, disease, and intercellular communication.严肃的纤毛:一个微小的细胞器照亮了进化、疾病和细胞间通讯。
Dev Cell. 2023 Aug 7;58(15):1333-1349. doi: 10.1016/j.devcel.2023.06.013. Epub 2023 Jul 24.
8
Deficiency of the Gene Causes Male Infertility with Morphological Abnormalities of the Sperm Flagellum in Mice.基因缺陷导致精子鞭毛形态异常的雄性不育症小鼠模型的建立。
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基于纤毛相关蛋白研究香烟烟雾诱导的大鼠气道炎症和精子活性损伤。

Investigating cigarette smoke-induced airway inflammation and sperm activity impairment in rats based on cilia-associated proteins.

作者信息

Wang Lei, Pan Min, Dong Jinhui, He Zengyang, Wang Wenbin, Shu Junsheng, Wang Tongsheng, Wang Yajuan

机构信息

Department of Physiology and Pharmacology, Anhui University of Chinese Medicine, Hefei, 230012 China.

Institutes of Physical Science and Information Technology, Anhui University, Hefei, 230061 China.

出版信息

3 Biotech. 2025 May;15(5):136. doi: 10.1007/s13205-025-04302-9. Epub 2025 Apr 19.

DOI:10.1007/s13205-025-04302-9
PMID:40260407
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12009257/
Abstract

The aim of this study was to investigate the mechanism of smoking-induced chronic obstructive pulmonary disease (COPD) and its impact on reproductive function in male rats and its relationship with chronic lung inflammation. The study used various methodologies including lung function tests, sperm quality assessment, serum hormone level measurement, and ultrastructural observations of airway cilia and sperm flagella to elucidate the effects of smoking on the reproductive and respiratory systems of rats. The results showed that smoking significantly induced lung damage and reduced sperm quality in rats, and the trend of lung damage and decreased sperm quality became more obvious with the increased duration of smoking. Transmission electron microscopy revealed that smoking exposure led to structural abnormalities of airway cilia and sperm flagella, and exposure after a period of three months showed significant damage to cilia and flagellar structures. Western blot and immunohistochemistry results indicated that the relative expression of NE proteins was significantly higher in the rats of the CS group, whereas the expression of FOXJ1 and SPAG6 proteins was notably lower in these rats after three months of smoking. In summary, smoke causes damage to the respiratory and reproductive systems of male rats, and the mechanism may be related to the destruction of airway cilia and sperm flagellar structures and the down-regulation of the expression of key ciliary proteins by smoke.

摘要

本研究旨在探讨吸烟诱导慢性阻塞性肺疾病(COPD)的机制及其对雄性大鼠生殖功能的影响,以及其与慢性肺部炎症的关系。该研究采用了多种方法,包括肺功能测试、精子质量评估、血清激素水平测定以及气道纤毛和精子鞭毛的超微结构观察,以阐明吸烟对大鼠生殖和呼吸系统的影响。结果表明,吸烟显著诱导大鼠肺损伤并降低精子质量,且随着吸烟时间的延长,肺损伤和精子质量下降的趋势变得更加明显。透射电子显微镜显示,吸烟暴露导致气道纤毛和精子鞭毛结构异常,暴露三个月后,纤毛和鞭毛结构出现明显损伤。蛋白质免疫印迹和免疫组织化学结果表明,香烟烟雾(CS)组大鼠中NE蛋白的相对表达显著更高,而吸烟三个月后,这些大鼠中FOXJ1和SPAG6蛋白的表达明显更低。总之,烟雾会对雄性大鼠的呼吸和生殖系统造成损害,其机制可能与气道纤毛和精子鞭毛结构的破坏以及烟雾导致关键纤毛蛋白表达下调有关。