Article3 Biotech2025
Investigating cigarette smoke-induced airway inflammation and sperm activity impairment in rats based on cilia-associated proteins.
Article in 3 Biotech, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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