PMID- 30116194
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1663-9812 (Print)
IS  - 1663-9812 (Electronic)
IS  - 1663-9812 (Linking)
VI  - 9
DP  - 2018
TI  - Ginsenoside Rg3 Attenuates Lipopolysaccharide-Induced Acute Lung Injury via 
      MerTK-Dependent Activation of the PI3K/AKT/mTOR Pathway.
PG  - 850
LID - 10.3389/fphar.2018.00850 [doi]
LID - 850
AB  - Acute lung injury (ALI) is a common clinical disease with high morbidity in both 
      humans and animals. Ginsenoside Rg3, a type of traditional Chinese medicine 
      extracted from ginseng, is widely used to cure many inflammation-related 
      diseases. However, the specific molecular mechanism of the effects of ginsenoside 
      Rg3 on inflammation has rarely been reported. Thus, we established a mouse model 
      of lipopolysaccharide (LPS)-induced ALI to investigate the immune protective 
      effects of ginsenoside Rg3 and explore its molecular mechanism. In wild type (WT) 
      mice, we found that ginsenoside Rg3 treatment significantly mitigated 
      pathological damages and reduced myeloperoxidase (MPO) activity as well as the 
      production of pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), 
      interleukin-1beta (IL-1beta) and interleukin-6 (IL-6); furthermore, the production of 
      anti-inflammatory mediators interleukin-10 (IL-10) and transforming growth 
      factor-beta (TGF-beta), polarization of M2 macrophages and expression levels of the 
      phosphorylation of phosphatidylinositol 3-hydroxy kinase (PI3K), protein kinase B 
      (PKB, also known as AKT), mammalian target of rapamycin (mTOR) and Mer receptor 
      tyrosine kinase (MerTK) were promoted. However, there were no significant 
      differences with regards to the pathological damage, MPO levels, inflammatory 
      cytokine levels, and protein expression levels of the phosphorylation of PI3K, 
      AKT and mTOR between the LPS treatment group and ginsenoside Rg3 group in 
      MerTK(-/-) mice. Taken together, the present study demonstrated that ginsenoside 
      Rg3 could attenuate LPS-induced ALI by decreasing the levels of pro-inflammatory 
      mediators and increasing the production of anti-inflammatory cytokines. These 
      processes were mediated through MerTK-dependent activation of its downstream the 
      PI3K/AKT/mTOR pathway. These findings identified a new site of the specific 
      anti-inflammatory mechanism of ginsenoside Rg3.
FAU - Yang, Jing
AU  - Yang J
AD  - State Key Laboratory of Agricultural Microbiology, College of Veterinary 
      Medicine, Huazhong Agricultural University, Wuhan, China.
FAU - Li, Senyang
AU  - Li S
AD  - State Key Laboratory of Agricultural Microbiology, College of Veterinary 
      Medicine, Huazhong Agricultural University, Wuhan, China.
FAU - Wang, Luyao
AU  - Wang L
AD  - State Key Laboratory of Agricultural Microbiology, College of Veterinary 
      Medicine, Huazhong Agricultural University, Wuhan, China.
FAU - Du, Fen
AU  - Du F
AD  - Hubei Center for Animal Diseases Control and Prevention, Wuhan, China.
FAU - Zhou, Xiaoliu
AU  - Zhou X
AD  - State Key Laboratory of Agricultural Microbiology, College of Veterinary 
      Medicine, Huazhong Agricultural University, Wuhan, China.
FAU - Song, Qiqi
AU  - Song Q
AD  - College of Animal Science and Veterinary Medicine, Tianjin Agricultural 
      University, Tianjin, China.
FAU - Zhao, Junlong
AU  - Zhao J
AD  - State Key Laboratory of Agricultural Microbiology, College of Veterinary 
      Medicine, Huazhong Agricultural University, Wuhan, China.
FAU - Fang, Rui
AU  - Fang R
AD  - State Key Laboratory of Agricultural Microbiology, College of Veterinary 
      Medicine, Huazhong Agricultural University, Wuhan, China.
LA  - eng
PT  - Journal Article
DEP - 20180802
PL  - Switzerland
TA  - Front Pharmacol
JT  - Frontiers in pharmacology
JID - 101548923
PMC - PMC6082957
OTO - NOTNLM
OT  - MerTK
OT  - acute lung injury
OT  - ginsenoside Rg3
OT  - inflammatory
OT  - lipopolysaccharide
EDAT- 2018/08/18 06:00
MHDA- 2018/08/18 06:01
PMCR- 2018/08/02
CRDT- 2018/08/18 06:00
PHST- 2018/04/13 00:00 [received]
PHST- 2018/07/13 00:00 [accepted]
PHST- 2018/08/18 06:00 [entrez]
PHST- 2018/08/18 06:00 [pubmed]
PHST- 2018/08/18 06:01 [medline]
PHST- 2018/08/02 00:00 [pmc-release]
AID - 10.3389/fphar.2018.00850 [doi]
PST - epublish
SO  - Front Pharmacol. 2018 Aug 2;9:850. doi: 10.3389/fphar.2018.00850. eCollection 
      2018.