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Published on: March 17, 2018
Paeoniflorin inhibits PDGF‑BB‑induced human airway smooth muscle cell growth and migration
Hong Zhou1, Qi Wu2, Luqing Wei3
1Graduate School of Tianjin Medical University, Tianjin 300070, P.R. China.
Abstract:
Abnormal proliferation and migration of airway smooth muscle cells (ASMCs) is important in the progression of asthma. Paeoniflorin (PF), one of the major active ingredients of Paeonia lactiflora, has been reported to exhibit anti‑asthmatic effects. However, the effects of PF in the regulation of platelet‑derived growth factor (PDGF)‑BB‑induced ASMC proliferation and migration remain unknown. The present study was designed to investigate the effects of PF on human ASMCs and the underlying mechanism. The results demonstrated that PF treatment significantly reduced the numbers of live ASMC cells and their PDGF‑BB‑induced migration. PF treatment also suppressed PDGF‑BB‑induced α‑smooth muscle actin expression in ASMCs. Furthermore, pretreatment with PF reduced PDGF‑BB‑induced phosphorylation of phosphoinositide 3‑kinase (PI3K) and AKT serine/threonine kinase 1 (Akt) in ASMCs. In conclusion, the present study demonstrated for the first time that PF inhibited ASMC growth and migration induced by PDGF‑BB, and that this effect may be partly due to inhibition of the PI3K/Akt signaling pathway. The results provide novel information regarding the role of PF as a potential therapeutic agent for the treatment of asthma.
Insights
Paeoniflorin (PF) effectively reduces airway smooth muscle cell proliferation and migration, key factors in asthma progression. This natural compound may offer a new therapeutic approach by inhibiting the PI3K/Akt signaling pathway.
Area of Science:
- Pharmacology
- Cell Biology
- Respiratory Medicine
Background:
- Airway smooth muscle cell (ASMC) proliferation and migration are critical in asthma pathogenesis.
- Paeoniflorin (PF), derived from Paeonia lactiflora, shows potential anti-asthmatic properties.
- The specific effects of PF on platelet-derived growth factor (PDGF)-BB-induced ASMC responses are not well understood.
Purpose of the Study:
- To investigate the inhibitory effects of PF on PDGF-BB-induced ASMC proliferation and migration.
- To elucidate the underlying molecular mechanisms of PF action in ASMCs.
Main Methods:
- Human ASMCs were treated with PF and/or PDGF-BB.
- Cell viability, proliferation, and migration assays were performed.
- Expression of alpha-smooth muscle actin (α-SMA) was assessed.
- Western blotting was used to detect the phosphorylation of PI3K and Akt.
Main Results:
- PF treatment significantly decreased ASMC viability and proliferation.
- PF inhibited PDGF-BB-induced ASMC migration.
- PF suppressed PDGF-BB-induced α-SMA expression.
- PF reduced PDGF-BB-induced phosphorylation of PI3K and Akt.
Conclusions:
- PF demonstrates significant inhibitory effects on ASMC proliferation and migration induced by PDGF-BB.
- The anti-asthmatic mechanism of PF may involve the inhibition of the PI3K/Akt signaling pathway.
- PF represents a potential therapeutic candidate for asthma treatment.
