PMID- 31912578
OWN - NLM
STAT- MEDLINE
DCOM- 20210729
LR  - 20221014
IS  - 1872-8081 (Electronic)
IS  - 0951-6433 (Linking)
VI  - 46
IP  - 5
DP  - 2020 Sep
TI  - Emodin relieved lipopolysaccharide-evoked inflammatory damage in WI-38 cells by 
      up-regulating taurine up-regulated gene 1.
PG  - 860-868
LID - 10.1002/biof.1609 [doi]
AB  - BACKGROUND: Neonatal pneumonia (NP) has a high fatality rate in neonatal illness. 
      This research investigated the functions of emodin on lipopolysaccharide 
      (LPS)-evoked inflammatory injury in WI-38 cells. METHODS: Cell counting kit-8 
      (CCK-8) assay and flow cytometry were utilized for examining the impacts of LPS 
      and emodin on viability and apoptosis, respectively. Taurine up-regulated gene 1 
      (TUG1) level was altered through cell transfection and investigated by reverse 
      transcription quantitative polymerase chain reaction (RT-qPCR). Moreover, 
      RT-qPCR, western blot and enzyme-linked immunosorbent assay (ELISA) were utilized 
      for investigating expressions of monocyte chemoattractant protein-1 (MCP-1) and 
      interleukin (IL)-6. Western blot was carried out for investigating the levels of 
      Bcl-2, Bax, pro-Caspase-3, cleaved-Caspase-3 and NF-kappaB and p38MAPK 
      pathway-related proteins. RESULTS: LPS treatment restrained cell viability, 
      enhanced apoptosis, and expressions of inflammation-related IL-6 and MCP-1. 
      Emodin alleviated LPS-evoked inflammatory injury and restrained the NF-kappaB and 
      p38MAPK pathways. Furthermore, emodin positively regulated TUG1 expression and 
      TUG1 silencing could reverse the efficacy of emodin on IL-6 and MCP-1 
      expressions. Finally, TUG1 regulates the expression of inflammatory factors 
      through NF-kappaB and p38MAPK pathways. CONCLUSION: Emodin alleviated LPS-evoked 
      inflammatory injury by raising TUG1 expression via NF-kappaB and p38MAPK pathways in 
      WI-38 cells.
CI  - (c) 2020 International Union of Biochemistry and Molecular Biology.
FAU - Zang, Linlin
AU  - Zang L
AD  - Department of Clinical Laboratory, The Affiliated Qingdao Hiser Hospital of 
      Qingdao University (Qingdao Hospital of Traditional Chinese Medicine), Qingdao, 
      China.
FAU - Song, Yongqing
AU  - Song Y
AD  - Department of Pharmaceutical, Binzhou People's Hospital, Binzhou, Shandong, 
      China.
FAU - Yu, Fengying
AU  - Yu F
AD  - Department of Pharmaceutical, Binzhou People's Hospital, Binzhou, Shandong, 
      China.
FAU - Liu, Xiuxia
AU  - Liu X
AUID- ORCID: 0000-0001-7392-3728
AD  - Department of Pediatrics, Jining No.1 People's Hospital, Jining, Shandong, China.
LA  - eng
PT  - Journal Article
PT  - Retracted Publication
DEP - 20200107
PL  - Netherlands
TA  - Biofactors
JT  - BioFactors (Oxford, England)
JID - 8807441
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (TUG1 long noncoding RNA, human)
RN  - 1EQV5MLY3D (Taurine)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - KA46RNI6HN (Emodin)
SB  - IM
RIN - Biofactors. 2023 Jan;49(1):193. PMID: 36239329
MH  - Apoptosis/drug effects
MH  - Cell Line
MH  - Cell Survival/drug effects
MH  - Chemokine CCL2/genetics
MH  - Emodin/*pharmacology
MH  - Humans
MH  - Inflammation/chemically induced/*drug therapy/genetics/pathology
MH  - Interleukin-6/genetics
MH  - Lipopolysaccharides/toxicity
MH  - NF-kappa B/genetics
MH  - RNA, Long Noncoding/antagonists & inhibitors/*genetics
MH  - Taurine/genetics
MH  - Transcriptional Activation/drug effects
MH  - p38 Mitogen-Activated Protein Kinases/*genetics
OTO - NOTNLM
OT  - NF-kappaB and p38MAPK pathways
OT  - TUG1
OT  - emodin
OT  - inflammatory damage
OT  - neonatal pneumonia
EDAT- 2020/01/09 06:00
MHDA- 2021/07/30 06:00
CRDT- 2020/01/09 06:00
PHST- 2019/09/30 00:00 [received]
PHST- 2019/12/19 00:00 [accepted]
PHST- 2020/01/09 06:00 [pubmed]
PHST- 2021/07/30 06:00 [medline]
PHST- 2020/01/09 06:00 [entrez]
AID - 10.1002/biof.1609 [doi]
PST - ppublish
SO  - Biofactors. 2020 Sep;46(5):860-868. doi: 10.1002/biof.1609. Epub 2020 Jan 7.