PMID- 32967760
OWN - NLM
STAT- MEDLINE
DCOM- 20201117
LR  - 20201117
IS  - 1007-8738 (Print)
IS  - 1007-8738 (Linking)
VI  - 36
IP  - 9
DP  - 2020 Sep
TI  - [Quorum sensing molecule N-3-oxodecanoyl-L-homoserine lactone (3-oxo-C(10)-HSL) 
      inhibits lipopolysaccharide-induced inflammatory responses of RAW264.7 
      macrophages].
PG  - 776-781
AB  - Objective To explore the regulatory effect of quorum sensing molecule 
      N-3-oxodecanoyl-L-homoserine lactone (3-oxo-C(10)-HSL) on lipopolysaccharide 
      (LPS)-induced inflammation in RAW264.7 macrophages. Methods RAW264.7 macrophages 
      were divided into experimental group, control group and blank group. The 
      experimental group was treated with different concentrations of 3-oxo-C(10)-HSL 
      and LPS; the control group was treated with DMSO and LPS; and the blank group was 
      treated with DMSO and PBS. Cells and supernatants were collected after 12 hours 
      of stimulation. The mRNA expression of interleukin-6 (IL-6), interleukin-1beta 
      (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and monocyte chemoattractant protein-1 
      (MCP-1) were detected by real-time quantitative PCR, and the protein levels of 
      IL-6 and TNF-alpha in supernatant were detected by ELSIA. Further, 25 mumol/L 
      3-oxo-C(10)-HSL and 100 ng/mL LPS were used to stimulate the cells for 15, 30 and 
      60 minutes, and the phosphorylation of nuclear factor kappaBp65 (NF-kappaBp65) was 
      detected by Western blot analysis. Results The 3-oxo-C(10)-HSL could decrease the 
      mRNA levels of IL-6, IL-1beta, TNF-alpha, MCP-1 and the protein levels of IL-6 and TNF-alpha 
      in LPS-treated RAW264.7 macrophages in a dose-dependent manner. In addition, 
      3-oxo-C(10)-HSL could inhibit the phosphorylation of NF-kappaBp65 induced by LPS. 
      Conclusion 3-oxo-C(10)-HSL can alleviate LPS-induced inflammatory responses in 
      RAW264.7 macrophages by inhibiting activation of NF-kappaB signaling pathway.
FAU - Qin, Kewei
AU  - Qin K
AD  - Central Laboratory, Sixth Medical Centre, Chinese People's Liberation Army 
      General Hospital, Beijing 100048, China.
FAU - Liu, Jianfei
AU  - Liu J
AD  - Central Laboratory, Sixth Medical Centre, Chinese People's Liberation Army 
      General Hospital, Beijing 100048, China.
FAU - Fu, Kaifei
AU  - Fu K
AD  - Central Laboratory, Sixth Medical Centre, Chinese People's Liberation Army 
      General Hospital, Beijing 100048, China.
FAU - Han, Shanqiao
AU  - Han S
AD  - Central Laboratory, Sixth Medical Centre, Chinese People's Liberation Army 
      General Hospital, Beijing 100048, China.
FAU - Chen, Xiuxiu
AU  - Chen X
AD  - Central Laboratory, Sixth Medical Centre, Chinese People's Liberation Army 
      General Hospital, Beijing 100048, China.
FAU - Zhou, Lijun
AU  - Zhou L
AD  - Central Laboratory, Sixth Medical Centre, Chinese People's Liberation Army 
      General Hospital, Beijing 100048, China. *Corresponding author, 
      E-mail:hzzhoulj@126.com.
LA  - chi
PT  - Journal Article
PL  - China
TA  - Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
JT  - Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular 
      immunology
JID - 101139110
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 1192-20-7 (homoserine lactone)
RN  - OL659KIY4X (4-Butyrolactone)
SB  - IM
MH  - 4-Butyrolactone/analogs & derivatives
MH  - Lipopolysaccharides
MH  - Macrophages
MH  - NF-kappa B
MH  - *Quorum Sensing
MH  - Tumor Necrosis Factor-alpha/genetics
EDAT- 2020/09/25 06:00
MHDA- 2020/11/18 06:00
CRDT- 2020/09/24 05:26
PHST- 2020/09/24 05:26 [entrez]
PHST- 2020/09/25 06:00 [pubmed]
PHST- 2020/11/18 06:00 [medline]
PST - ppublish
SO  - Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2020 Sep;36(9):776-781.