Naringenin Targets PI3K p85alpha to Suppress PI3K/AKT Signaling Pathway and Ameliorate Disordered MMP-9 Secretion in Cigarette Smoke Extract-Induced Alveolar Macrophages In Vitro DOI Creative Commons
Weiyang Fan,

Ziyan Xu,

Mengli Zhong

et al.

Cells, Journal Year: 2025, Volume and Issue: 14(10), P. 678 - 678

Published: May 8, 2025

Background: Naringenin has demonstrated potential therapeutic effects against cigarette smoke-induced lung injury; however, its underlying mechanisms of regulating matrix metalloproteinase-9 (MMP-9) in alveolar macrophages remain unclear. Methods: The regulatory naringenin smoke extract (CSE)-induced were investigated using proteomics, and then, naringenin’s targets further validated by Western blot, molecular docking, dynamics (MD) simulations, cellular thermal shift assay (CETSA), enzyme activity assay. Results: proteomics revealed that the PI3K/AKT signaling pathway might play a crucial role inhibition MMP-9. blot analysis confirmed significantly inhibited CSE-upregulated reduced MMP-9 expression MH-S cells. Notably, PI3K activator 740Y-P reversed on Additionally, MD CETSA identified p85alpha as binding site for naringenin, markedly CSE-induced activity. In vitro experiments, inhibiting secretion contributed to alleviating elastin E-cadherin damage epithelial Furthermore, effectively suppressed primary mouse human THP-1-differentiated macrophages. Conclusions: Our findings candidate treating smoking-induced injury, directly targeted p85alpha, via suppressing pathway.

Language: Английский

The mechanism of egg production improvement in laying hens before and after molting revealed by transcriptome and metabolome integration DOI Creative Commons

Mengqing Sun,

Hailing Wang,

Xinyu Zhu

et al.

Poultry Science, Journal Year: 2025, Volume and Issue: unknown, P. 105125 - 105125

Published: April 1, 2025

The objective of this research was to examine the effects and underlying mechanisms forced molting on laying rate hens. A total ninety 500-day-old hens were randomly assigned three groups: a control group (CK), starvation (SG), recovery (RG). study evaluated follicular development in measured expression levels antioxidant, lipid, inflammatory factors their serum. Additionally, transcriptomic metabolomic analyses performed assess gene metabolic profiles findings indicated that led an increase rates, reduction closure, significant rise antioxidant enzymes such as GSH, CAT, SOD, alongside decrease MDA levels. Furthermore, there reductions blood lipid LDL, HDL, TC, TG. notable differences markers TNF-α, IL-1, IL-6. data revealed influenced activation PI3K-AKT mTOR signaling pathways, affecting fatty acid metabolism modulating associated genes. In conclusion, demonstrates is effective strategy for enhancing it provides valuable theoretical framework advancing breeding practices aimed at improving egg production.

Language: Английский

Citations

0
Naringenin Targets PI3K p85alpha to Suppress PI3K/AKT Signaling Pathway and Ameliorate Disordered MMP-9 Secretion in Cigarette Smoke Extract-Induced Alveolar Macrophages In Vitro DOI Creative Commons
Weiyang Fan,

Ziyan Xu,

Mengli Zhong

et al.

Cells, Journal Year: 2025, Volume and Issue: 14(10), P. 678 - 678

Published: May 8, 2025

Background: Naringenin has demonstrated potential therapeutic effects against cigarette smoke-induced lung injury; however, its underlying mechanisms of regulating matrix metalloproteinase-9 (MMP-9) in alveolar macrophages remain unclear. Methods: The regulatory naringenin smoke extract (CSE)-induced were investigated using proteomics, and then, naringenin’s targets further validated by Western blot, molecular docking, dynamics (MD) simulations, cellular thermal shift assay (CETSA), enzyme activity assay. Results: proteomics revealed that the PI3K/AKT signaling pathway might play a crucial role inhibition MMP-9. blot analysis confirmed significantly inhibited CSE-upregulated reduced MMP-9 expression MH-S cells. Notably, PI3K activator 740Y-P reversed on Additionally, MD CETSA identified p85alpha as binding site for naringenin, markedly CSE-induced activity. In vitro experiments, inhibiting secretion contributed to alleviating elastin E-cadherin damage epithelial Furthermore, effectively suppressed primary mouse human THP-1-differentiated macrophages. Conclusions: Our findings candidate treating smoking-induced injury, directly targeted p85alpha, via suppressing pathway.

Language: Английский

Citations

0