ArticleRespiratory research2025
Yanghe Pingchuan granules inhibit cellular senescence in airway smooth muscle cells to improve bronchial asthma via modulating Nrf2 acetylation.
Article in Respiratory research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Efficacy of Yupingfeng powder in the treatment of bronchial asthma in adults: a systematic review and meta-analysis.Frontiers in pharmacology · 2026Pooled it
- The Role of Cellular Senescence in Obstructive Airway Diseases: From Mechanisms to Therapeutic Targets.International journal of molecular sciences · 2026Review
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Abstract
backgroundBronchial asthma (BA) is regarded as one of the most prevalent chronic respiratory diseases worldwide. Yanghe Pingchuan Granules (YPG), a traditional Chinese medicine (TCM) compound, has been employed extensively in treating BA. However, the precise mechanism by which it exerts its therapeutic effects remains to be fully elucidated. This study aimed to investigate the therapeutic mechanisms of YPG in BA model rats, focusing on the interventional effects on cellular senescence of airway smooth muscle cells (ASMCs) in vivo and in vitro.
methodsIn this study, OVA was utilized to induce the replication of an asthmatic rat model, α-smooth muscle actin (α-SMA) was employed to identify ASMCs, and a series of in vitro experiments were conducted. These experiments included β-galactosidase (β-gal), Enzyme-linked immunosorbent assay (ELISA), biochemical assay, western blotting, Co-Immunoprecipitation (CO-IP), overexpression/silencing of Sirtuin 1 (SIRT1) and Nuclear factor E2-related factor 2 (Nrf2) was studied in ASMCs. Subsequently, Hematoxylin and Eosin (H&E), Masson, Alcian Blue-Periodic Acid Schiff (AB-PAS), ELISA, biochemical assay, western blotting, Co-Immunofluorescence (CO-IF), and CO-IP were employed to examine the histopathological damage, acetylation, oxidative stress, senescence-related protein expression, and senescence-associated secretion phenotype (SASP) secretion of bronchial tubes in asthmatic rats. This comprehensive approach was undertaken to elucidate the mechanism by which YPG inhibits the senescence of ASMCs.
resultsThe results of in vivo and in vitro experiments demonstrated that SIRT1 overexpression and YPG inhibited the senescence of ASMCs and significantly reduced P16 and P21 proteins, as well as cellular SASP (Interleukin-1β (IL-1β), Interleukin-4 (IL-4), and Interleukin-17 (IL-17)). Moreover, YPG demonstrated a substantial reduction in histopathological alterations in BA rats. Furthermore, the study observed a decline in Malondialdehyde (MDA) expression, concomitant with an augmentation in the expression levels of SIRT1, Nrf2, oxygenase-1 (HO-1), Superoxide dismutase (SOD), and Catalase (CAT). It substantiated the interaction of SIRT1 with Nrf2 and the decrease in the expression level of Nrf2 acetylation.
conclusionsThese results suggest that YPG can activate the SIRT1/Nrf2/HO-1 signaling pathway by regulating the expression level of SIRT1 to regulating the acetylated expression level of Nrf2, to inhibit the senescence of ASMCs, leading to the treatment of asthma.
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