PMID- 35994826
OWN - NLM
STAT- MEDLINE
DCOM- 20220908
LR  - 20221007
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 626
DP  - 2022 Oct 20
TI  - Butyrolactone I attenuates inflammation in murine NASH by inhibiting the NF-kappaB 
      signaling pathway.
PG  - 167-174
LID - S0006-291X(22)01019-1 [pii]
LID - 10.1016/j.bbrc.2022.07.050 [doi]
AB  - Nonalcoholic steatohepatitis (NASH) is the development of non-alcoholic fatty 
      liver disease (NAFLD) and a key element in the exacerbation of NAFLD. Since there 
      are currently no drugs approved by the U.S. Food and Drug Administration to treat 
      this disease, the search for treatments that can be translated into clinical use 
      is urgent. Butyrolactone I (BLI), isolated from Aspergillus terreus, is an active 
      compound possessing multiple biological activities. However, the effects of BLI 
      on NASH have never been reported. In this study, RAW264.7 cells stimulated by 
      lipopolysaccharide (LPS) were applied to study the anti-inflammatory effect and 
      the underlying mechanisms of BLI in vitro. Following this, mice fed with high-fat 
      and -fructose diet (HFFD) were used to explore the alleviation of NASH by 
      BLIin vivo. We found that BLI attenuated inflammation in LPS-induced 
      RAW264.7 cells by inhibiting the NF-kappaB signaling pathway and downregulating the 
      expression of iNOS and COX-2. Moreover, results of experiments in vivo 
      demonstrated that BLI reduced serum transaminase levels, decreased hepatic fat 
      accumulation, inhibited inflammation, suppressed oxidative stress, and 
      ameliorated liver fibrosis. For the first time, we investigated the role of BLI 
      in the treatment of murine NASH. We found that BLI alleviates NASH partly by 
      inhibiting the NF-kappaB pathway of signaling. Given its hepatoprotective effects and 
      non-toxic properties, BLI can be a novel and effective drug for NASH patients.
CI  - Copyright (c) 2022 The Authors. Published by Elsevier Inc. All rights reserved.
FAU - Tian-Qi, Chen
AU  - Tian-Qi C
AD  - Medical College, China Three Gorges University and Hubei Key Laboratory of Tumor 
      Microenvironment and Immunotherapy, China Three Gorges University, Yichang, 
      443003, China.
FAU - Yan-Fang, Deng
AU  - Yan-Fang D
AD  - Hubei Key Laboratory of Natural Medicinal Chemistry and Resource Evaluation, 
      School of Pharmacy, Tongji Medical College, Huazhong University of Science and 
      Technology, Wuhan, 430030, China.
FAU - Yan-Yan, Wang
AU  - Yan-Yan W
AD  - Medical College, China Three Gorges University and Hubei Key Laboratory of Tumor 
      Microenvironment and Immunotherapy, China Three Gorges University, Yichang, 
      443003, China. Electronic address: wangyy1001@163.com.
FAU - Yong-Hui, Zhang
AU  - Yong-Hui Z
AD  - Hubei Key Laboratory of Natural Medicinal Chemistry and Resource Evaluation, 
      School of Pharmacy, Tongji Medical College, Huazhong University of Science and 
      Technology, Wuhan, 430030, China. Electronic address: zhangyh@mails.tjmu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20220811
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 87414-49-1 (butyrolactone I)
RN  - OL659KIY4X (4-Butyrolactone)
SB  - IM
MH  - 4-Butyrolactone/analogs & derivatives
MH  - Animals
MH  - Disease Models, Animal
MH  - Inflammation/drug therapy/metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Liver/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - NF-kappa B/metabolism
MH  - *Non-alcoholic Fatty Liver Disease/drug therapy/metabolism
MH  - Signal Transduction
OTO - NOTNLM
OT  - Butyrolactone I
OT  - Inflammation
OT  - NF-kappaB signaling pathway
OT  - Nonalcoholic steatohepatitis
COIS- Declaration of competing interest The authors declare no conflict of interest.
EDAT- 2022/08/23 06:00
MHDA- 2022/09/09 06:00
CRDT- 2022/08/22 18:14
PHST- 2022/07/08 00:00 [received]
PHST- 2022/07/14 00:00 [accepted]
PHST- 2022/08/23 06:00 [pubmed]
PHST- 2022/09/09 06:00 [medline]
PHST- 2022/08/22 18:14 [entrez]
AID - S0006-291X(22)01019-1 [pii]
AID - 10.1016/j.bbrc.2022.07.050 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2022 Oct 20;626:167-174. doi: 
      10.1016/j.bbrc.2022.07.050. Epub 2022 Aug 11.