Induction of chronic asthma up regulated the transcription of senile factors in male rats.

IF 2.4 3区生物学 Q4 CELL BIOLOGY

BMC Molecular and Cell Biology Pub Date : 2024-10-18 DOI:10.1186/s12860-024-00518-4

Majid Hassanzadeh-Khanmiri, Rana Keyhanmanesh, Reza Mosaddeghi-Heris, Aref Delkhosh, Jafar Rezaie, Sajjad Taghizadeh, Mehdi Rezai Seghin Sara, Mahdi Ahmadi

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Abstract

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.

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诱发慢性哮喘会上调雄性大鼠体内衰老因子的转录。

背景：哮喘的主要特征是慢性炎症：哮喘的主要特征是慢性炎症。我们通过组织学和分子测定法对哮喘模型大鼠肺部的细胞衰老进行了研究。该模型包括通过多次腹腔注射含氢氧化铝的卵清蛋白进行致敏，然后每隔一天进行一次气溶胶挑战：数据显示，哮喘诱导引起的组织学变化包括胸膜充血、间质性肺炎、纤维蛋白原凝块和炎症细胞聚集。哮喘组 IL-1β 和 NF-kB 蛋白升高（P综上所述，这些研究结果表明，哮喘会加速肺组织细胞的衰老。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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