PMID- 33039959
OWN - NLM
STAT- MEDLINE
DCOM- 20210525
LR  - 20211204
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 89
IP  - Pt A
DP  - 2020 Dec
TI  - Nervilifordin F alleviates intestinal ischemia/reperfusion-induced acute lung 
      injury via inhibiting inflammasome and mTOR pathway.
PG  - 107014
LID - S1567-5769(20)32149-4 [pii]
LID - 10.1016/j.intimp.2020.107014 [doi]
AB  - Acute lung injury (ALI) is a life-threatening disorder with high rates of 
      morbidity and mortality. Up to now, there are still no effective drugs for its 
      therapies due to the complexity of its etiology and pathogenesis. In this present 
      study, we investigated the protective effect of Nervilifordin F (NF) on ALI 
      induced by intestinal ischemia/reperfusion (II/R) and its related mechanism. 
      Firstly, the ALI model rats were induced through II/R, and treated with NF. Then, 
      the pathological and cytokine level changes in the lung tissue of ALI rats were 
      evaluated by hematoxylin and eosin and enzyme-linked immunosorbent assay (ELISA). 
      The related genes expression level of mammalian target of rapamycin (mTOR) 
      pathway and inflammasome were measured by real-time quantitative polymerase chain 
      reaction (RT-qPCR), western blot and immunohistochemistry. Finally, the 
      NF-protein complexes were predicted by SYBYL-X 2.0. The results indicated that NF 
      can significant reduces the levels of tumor necrosis factor-alpha (TNF-alpha), 
      interleukin (IL)-6 and IL-1beta, and inhibits the expression of inflammasome related 
      genes (such as toll-like receptor 4 (TLR4), p65, NOD-like receptor protein 3 
      (NLRP3) and Caspase 1), thereby reduce inflammation in II/R-induced ALI rats. 
      Moreover, NF can activate the expression of FK506 binding protein 25 (FKBP25) and 
      down-regulate the expression of mTOR and p70 ribosomal protein S6 kinase 1 
      (p70S6K). In addition, molecular docking results showed that NF can be combined 
      well with p70S6K, TLR4, mTOR and NLRP3, which further verified the inhibitory 
      effect of NF on ALI inflammation. Therefore, the findings indicate that NF can 
      alleviates II/R-induced inflammation of ALI rats by inhibiting inflammasome 
      related genes and mTOR pathway, which expected to use as a potential drug for the 
      treatment of ALI.
CI  - Copyright (c) 2020 Elsevier B.V. All rights reserved.
FAU - Tan, Yanjun
AU  - Tan Y
AD  - College of Pharmacy, Guangxi Medical University, Nanning, Guangxi, China.
FAU - Zuo, Wenpu
AU  - Zuo W
AD  - Life Science Institute, Guangxi Medical University, Nanning, Guangxi, China.
FAU - Huang, Lingling
AU  - Huang L
AD  - College of Pharmacy, Guangxi Medical University, Nanning, Guangxi, China; The 
      First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China; 
      Langdong Hospital of Guangxi Medical University, Nanning, Guangxi, China.
FAU - Zhou, Bo
AU  - Zhou B
AD  - Scientific Research Center, Guilin Medical University, Guilin, Guangxi, China.
FAU - Liang, Hui
AU  - Liang H
AD  - College of Pharmacy, Guangxi Medical University, Nanning, Guangxi, China.
FAU - Zheng, Shengfeng
AU  - Zheng S
AD  - The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 
      China.
FAU - Jia, Wenxian
AU  - Jia W
AD  - College of Pharmacy, Guangxi Medical University, Nanning, Guangxi, China.
FAU - Chen, Suixia
AU  - Chen S
AD  - Department of Pathophysiology, Guangxi Medical University, Nanning, Guangxi, 
      China.
FAU - Liu, Jiayi
AU  - Liu J
AD  - The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 
      China.
FAU - Yang, Xiaoli
AU  - Yang X
AD  - College of Pharmacy, Guangxi Medical University, Nanning, Guangxi, China; 
      Scientific Research Center, Guilin Medical University, Guilin, Guangxi, China. 
      Electronic address: cncsyxl@glmc.edu.cn.
FAU - Jiao, Yang
AU  - Jiao Y
AD  - College of Pharmacy, Guangxi Medical University, Nanning, Guangxi, China. 
      Electronic address: jiaoyanggx@163.com.
LA  - eng
PT  - Journal Article
DEP - 20201008
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Cytokines)
RN  - 0 (Inflammasomes)
RN  - 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
RN  - 0 (Nlrp3 protein, rat)
RN  - 0 (Rela protein, rat)
RN  - 0 (Transcription Factor RelA)
RN  - EC 2.7.1.1 (mTOR protein, rat)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Acute Lung Injury/enzymology/etiology/pathology/*prevention & control
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Cytokines/genetics/metabolism
MH  - Disease Models, Animal
MH  - Gene Expression Regulation
MH  - Inflammasomes/genetics/*metabolism
MH  - Intestinal Diseases/complications/*drug therapy/enzymology/pathology
MH  - Lung/*drug effects/enzymology/pathology
MH  - Male
MH  - Molecular Docking Simulation
MH  - NLR Family, Pyrin Domain-Containing 3 Protein/genetics/*metabolism
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury/complications/*drug therapy/enzymology/pathology
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/*metabolism
MH  - Transcription Factor RelA/genetics/metabolism
OTO - NOTNLM
OT  - Acute lung injury
OT  - Intestinal ischemia/reperfusion
OT  - Nervilifordin F
OT  - mTOR
EDAT- 2020/10/12 06:00
MHDA- 2021/05/26 06:00
CRDT- 2020/10/11 20:34
PHST- 2020/06/28 00:00 [received]
PHST- 2020/09/13 00:00 [revised]
PHST- 2020/09/13 00:00 [accepted]
PHST- 2020/10/12 06:00 [pubmed]
PHST- 2021/05/26 06:00 [medline]
PHST- 2020/10/11 20:34 [entrez]
AID - S1567-5769(20)32149-4 [pii]
AID - 10.1016/j.intimp.2020.107014 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2020 Dec;89(Pt A):107014. doi: 10.1016/j.intimp.2020.107014. 
      Epub 2020 Oct 8.