Feedback

Erythromycin attenuates oxidative stress-induced cellular senescence via the PI3K-mTOR signaling pathway in chronic obstructive pulmonary disease

Affiliation
Department of Respiratory and Critical Medicine ,The First Affiliated Hospital of Guangxi Medical University ,Nanning ,Guangxi ,China
Xiaofei, Yi;
Affiliation
Department of Respiratory and Critical Medicine ,The First Affiliated Hospital of Guangxi Medical University ,Nanning ,Guangxi ,China
Tingting, Li;
Affiliation
Department of Respiratory and Critical Medicine ,The First Affiliated Hospital of Guangxi Medical University ,Nanning ,Guangxi ,China
Xuan, Wei;
Affiliation
Department of Respiratory and Critical Medicine ,The First Affiliated Hospital of Guangxi Medical University ,Nanning ,Guangxi ,China
Zhiyi, He

Background and Purpose: Chronic obstructive pulmonary disease (COPD) is proposed to hasten lung aging. Erythromycin protects against oxidative stress and inflammatory responses. However, the potential anti-senescence effect of erythromycin remains disclosed. In the present study, we investigated whether erythromycin influenced oxidative stress-induced cellular senescence and investigated its related mechanisms. Methods: A cigarrete smoke (CS) -induced emphysema mouse model and a H 2 O 2 -induced premature senescence model in human bronchial epithelial cell line (BEAS-2B) were established. Senescence-related markers (P53, P21 and SA-β-Gal activity), and levels of oxidative stress biomarkers (MDA, SOD and ROS) were measured. Additionally, cells were pretreated with rapamycin (mTOR inhibitor) or erythromycin, and the expression levels of components of the PI3K-mTOR signaling pathway were measured in BEAS-2B cells. Results: Exposed to H 2 O 2 , increased SA-β-gal activity was observed in BEAS-2B cells suggesting premature senescence. Erythromycin inhibited the expression of P53 and P21 in the CS-induced emphysema mouse model. MDA levels significantly increased and SOD levels decreased in the CS-exposed mice and H 2 O 2 -induced BEAS-2B cells. Rapamycin and erythromycin significantly suppressed the expression of P53 and P21. Additionally, rapamycin and erythromycin inhibited the PI3K-mTOR signaling pathway. Conclusion: Our findings suggest that erythromycin ameliorates oxidative stress-induced cellular senescence via the PI3K-mTOR signaling pathway. Hence, we establish a theoretical foundation for the clinical application of erythromycin for COPD prevention and treatment.

Cite

Citation style:
Could not load citation form.

Access Statistic

Total:
Downloads:
Abtractviews:
Last 12 Month:
Downloads:
Abtractviews:

Rights

License Holder: Copyright © 2022 Xiaofei, Tingting, Xuan and Zhiyi.

Use and reproduction: