TY - JOUR
T1 - Yupingfeng San Inhibits NLRP3 Inflammasome to Attenuate the Inflammatory Response in Asthma Mice
AU - Liu, Xue
AU - Shen, Jiawen
AU - Fan, Danping
AU - Qiu, Xuemei
AU - Guo, Qingqing
AU - Zheng, Kang
AU - Luo, Hui
AU - Shu, Jun
AU - Lu, Cheng
AU - Zhang, Ge
AU - Lu, Aiping
AU - Ma, Chaoying
AU - He, Xiaojuan
N1 - Funding Information:
This study was supported by the research funding from Ministry of Sciences and Technology of China (No. 2014DFG32700) and Hong Kong Baptist University Strategic Development Fund (SDF15-0324-P02(b)).
Publisher copyright:
© 2017 Liu, Shen, Fan, Qiu, Guo, Zheng, Luo, Shu, Lu, Zhang, Lu, Ma and He.
PY - 2017/12/22
Y1 - 2017/12/22
N2 - Yupingfeng San (YPFS) is a representative Traditional Chinese Medicine (TCM) formula with accepted therapeutic effect on Asthma. However, its action mechanism is still obscure. In this study, we used network pharmacology to explore potential mechanism of YPFS on asthma. Nucleotide-binding oligomerization domain (NOD)-like receptor pathway was shown to be the top one shared signaling pathway associated with both YPFS and asthma. In addition, NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome was treated as target protein in the process of YPFS regulating asthma. Further, experimental validation was done by using LPS-stimulated U937 cells and ovalbumin (OVA)-sensitized BALB/c mice model. In vitro experiments showed that YPFS significantly decreased the production of TNF-α and IL-6, as well as both mRNA and protein levels of IL-1β, NLRP3, Caspase-1 and ASC in LPS-stimulated U937 cells. In vivo experiment indicated that YPFS treatment not only attenuated the clinical symptoms, but also reduced inflammatory cell infiltration, mucus secretion and MUC5AC production in lung tissue of asthmatic mice. Moreover, YPFS treatment remarkably decreased the mRNA and protein levels of IL-1β, NLRP3, Caspase-1 and ASC in lung tissue of asthmatic mice. In conclusion, these results demonstrated that YPFS could inhibit NLRP3 inflammasome components to attenuate the inflammatory response in asthma.
AB - Yupingfeng San (YPFS) is a representative Traditional Chinese Medicine (TCM) formula with accepted therapeutic effect on Asthma. However, its action mechanism is still obscure. In this study, we used network pharmacology to explore potential mechanism of YPFS on asthma. Nucleotide-binding oligomerization domain (NOD)-like receptor pathway was shown to be the top one shared signaling pathway associated with both YPFS and asthma. In addition, NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome was treated as target protein in the process of YPFS regulating asthma. Further, experimental validation was done by using LPS-stimulated U937 cells and ovalbumin (OVA)-sensitized BALB/c mice model. In vitro experiments showed that YPFS significantly decreased the production of TNF-α and IL-6, as well as both mRNA and protein levels of IL-1β, NLRP3, Caspase-1 and ASC in LPS-stimulated U937 cells. In vivo experiment indicated that YPFS treatment not only attenuated the clinical symptoms, but also reduced inflammatory cell infiltration, mucus secretion and MUC5AC production in lung tissue of asthmatic mice. Moreover, YPFS treatment remarkably decreased the mRNA and protein levels of IL-1β, NLRP3, Caspase-1 and ASC in lung tissue of asthmatic mice. In conclusion, these results demonstrated that YPFS could inhibit NLRP3 inflammasome components to attenuate the inflammatory response in asthma.
KW - Asthma
KW - Inflammation
KW - Network pharmacology
KW - NLRP3 inflammasome
KW - Yupingfeng San
UR - http://www.scopus.com/inward/record.url?scp=85039035923&partnerID=8YFLogxK
U2 - 10.3389/fphar.2017.00944
DO - 10.3389/fphar.2017.00944
M3 - Journal article
AN - SCOPUS:85039035923
SN - 1663-9812
VL - 8
JO - Frontiers in Pharmacology
JF - Frontiers in Pharmacology
M1 - 944
ER -
