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2016 ; 19
(9
): 993-1002
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Anti-inflammatory effect of Yu-Ping-Feng-San via TGF-?1 signaling suppression in
rat model of COPD
#MMPMID27803787
Yang ZS
; Yan JY
; Han NP
; Zhou W
; Cheng Y
; Zhang XM
; Li N
; Yuan JL
Iran J Basic Med Sci
2016[Sep]; 19
(9
): 993-1002
PMID27803787
show ga
OBJECTIVES: Yu-Ping-Feng-San (YPFS) is a classical traditional Chinese medicine
that is widely used for treatment of the diseases in respiratory systems,
including chronic obstructive pulmonary disease (COPD) recognized as chronic
inflammatory disease. However, the molecular mechanism remains unclear. Here we
detected the factors involved in transforming growth factor beta 1 (TGF-?1)/Smad2
signaling pathway and inflammatory cytokines, to clarify whether YPFS could
attenuate inflammatory response dependent on TGF-?1/Smad2 signaling in COPD rats
or cigarette smoke extract (CSE)-treated human bronchial epithelial (Beas-2B)
cells. MATERIALS AND METHODS: The COPD rat model was established by exposure to
cigarette smoke and intratracheal instillation of lipopolysaccharide, YPFS was
administered to the animals. The efficacy of YPFS was evaluated by comparing the
severity of pulmonary pathological damage, pro-inflammation cytokines, collagen
related genes and the activation of TGF-?1/Smad2 signaling pathway. Furthermore,
CSE-treated cells were employed to confirm whether the effect of YPFS was
dependent on the TGF-?1/Smad2 signaling via knockdown Smad2 (Si-RNA), or
pretreatment with the inhibitor of TGF-?1. RESULTS: Administration of YPFS
effectively alleviated injury of lung, suppressed releasing of pro-inflammatory
cytokines and collagen deposition in COPD animals (P<0.05), whereas exogenous
TGF-?1 promoted releasing of IL-1?, IL-6, TNF? (P<0.05). Administration YPFS
reduced inflammatory response significantly, also down-regulated TGF-?1/Smad2
signaling in vivo and in vitro. Unexpectedly, knockdown Smad2 or inhibition of
TGF-?1 abolished anti-inflammatory effect of YPFS in CSE-treated cells.
CONCLUSION: YPFS accomplished anti-inflammatory effects mainly by suppressing
phosphorylation of Smad2, TGF-?1/Smad2 signaling pathway was required for
YPFS-mediated anti-inflammation in COPD rats or CSE-treated Beas-2B cells.
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