诱导慢性哮喘上调了雄性大鼠衰老因子的转录。
Induction of chronic asthma up regulated the transcription of senile factors in male rats.
机构信息
Tuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
出版信息
BMC Mol Cell Biol. 2024 Oct 18;25(1):23. doi: 10.1186/s12860-024-00518-4.
BACKGROUND
The main characteristic of asthma is chronic inflammation. We examined cellular senescence by histology and molecular assay in the lungs of a rat model of asthma. This model comprises sensitization by several intraperitoneal injections of ovalbumin with aluminium hydroxide, followed by aerosol challenges every other day.
RESULTS
Data showed that asthma induction caused histological changes including, hyperemia, interstitial pneumonia, fibrinogen clots, and accumulation of inflammatory cells in the pleura. There is an elevation of IL-1β and NF-kB proteins in the asthmatic group (P < 0.001) compared to the control group. The expression of ß-galactosidase increased (P < 0.01), while the expression of Klotho and Sox2 genes was decreased in the lung tissue of the asthmatic group (P < 0.01).
CONCLUSION
Taken together, these findings suggest that asthmatic conditions accelerated the cellular senescence in the lung tissue.
背景
哮喘的主要特征是慢性炎症。我们通过组织学和分子检测检查了哮喘大鼠模型肺部的细胞衰老。该模型包括用氢氧化铝多次腹腔注射卵清蛋白进行致敏，然后每隔一天进行雾化挑战。
结果
数据显示，哮喘诱导引起了组织学变化，包括充血、间质性肺炎、纤维蛋白凝块和胸膜中炎症细胞的积累。与对照组相比，哮喘组的 IL-1β 和 NF-kB 蛋白水平升高（P<0.001）。β-半乳糖苷酶的表达增加（P<0.01），而哮喘组肺组织中 Klotho 和 Sox2 基因的表达减少（P<0.01）。
结论
综上所述，这些发现表明哮喘状态加速了肺组织中的细胞衰老。
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