PMID- 34678721
OWN - NLM
STAT- MEDLINE
DCOM- 20220125
LR  - 20220125
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 144
DP  - 2021 Dec
TI  - Potentilla discolor ameliorates LPS-induced inflammatory responses through 
      suppressing NF-kappaB and AP-1 pathways.
PG  - 112345
LID - S0753-3322(21)01129-X [pii]
LID - 10.1016/j.biopha.2021.112345 [doi]
AB  - Potentilla discolor Bunge (PD) is a traditional Chinese medicine which has been 
      widely used for the treatment of various inflammatory diseases (e.g., diarrhea, 
      fever and furuncle). However, few studies focused on its effect on classical 
      inflammation. This study aimed to investigate the anti-inflammatory effect and 
      potential mechanism of the ethanol extract of the whole herbs of PD (EPD) in 
      lipopolysaccharide (LPS)-induced inflammatory models. The obtained results showed 
      that EPD decreased supernatant NO, tumor necrosis factor-alpha (TNF-alpha) and monocyte 
      chemoattractant protein-1 (MCP-1) in LPS-activated RAW264.7 cells and mouse 
      peritoneal macrophages. Moreover, its effect on NO was attributed to the 
      suppression of iNOS expression rather than its activity. At the transcriptional 
      level, EPD suppressed iNOS, TNF-alpha and MCP-1 mRNA expressions in LPS-stimulated 
      RAW264.7 cells. Further study showed that EPD didn't affect the phosphorylation 
      and degradation of IkappaBalpha, but yet impeded the nuclear translocation of p65 to 
      inhibit NF-kappaB activation. Meanwhile, it also prevented JNK, ERK1/2 and p38 
      phosphorylation to dampen the activation of AP-1. In endotoxemia mouse model, EPD 
      not only decreased interleukin-6, TNF-alpha and MCP-1 levels in serum, but also 
      potently ameliorated diarrhea. These findings provide the theoretical basis for 
      PD to treat inflammatory diseases, especially intestinal inflammation.
CI  - Copyright (c) 2021 The Authors. Published by Elsevier Masson SAS.. All rights 
      reserved.
FAU - Zhang, Xiaoyu
AU  - Zhang X
AD  - Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & 
      Peking Union Medical College, Beijing 100193, China.
FAU - Kang, Yuan
AU  - Kang Y
AD  - Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & 
      Peking Union Medical College, Beijing 100193, China.
FAU - Li, Ximeng
AU  - Li X
AD  - Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & 
      Peking Union Medical College, Beijing 100193, China.
FAU - Huang, Yunfeng
AU  - Huang Y
AD  - Guangxi Institute of Chinese Medicine & Pharmaceutical Science, Nanning 530022, 
      Guangxi, China.
FAU - Qi, Ruijuan
AU  - Qi R
AD  - Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & 
      Peking Union Medical College, Beijing 100193, China.
FAU - Han, Yixin
AU  - Han Y
AD  - Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & 
      Peking Union Medical College, Beijing 100193, China.
FAU - Cai, Runlan
AU  - Cai R
AD  - Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & 
      Peking Union Medical College, Beijing 100193, China.
FAU - Gao, Yuan
AU  - Gao Y
AD  - Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & 
      Peking Union Medical College, Beijing 100193, China. Electronic address: 
      ygao@implad.ac.cn.
FAU - Qi, Yun
AU  - Qi Y
AD  - Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & 
      Peking Union Medical College, Beijing 100193, China. Electronic address: 
      yqi@implad.ac.cn.
LA  - eng
PT  - Journal Article
DEP - 20211019
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Nfkbia protein, mouse)
RN  - 0 (Plant Extracts)
RN  - 0 (Tnf protein, mouse)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 139874-52-5 (NF-KappaB Inhibitor alpha)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.13.39 (Nos2 protein, mouse)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/isolation & purification/*pharmacology
MH  - Chemokine CCL2/genetics/metabolism
MH  - Diarrhea/chemically induced/immunology/metabolism/prevention & control
MH  - Disease Models, Animal
MH  - Endotoxemia/chemically induced/immunology/metabolism/*prevention & control
MH  - Inflammation/chemically induced/immunology/metabolism/*prevention & control
MH  - Lipopolysaccharides
MH  - Macrophages/*drug effects/immunology/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred ICR
MH  - NF-KappaB Inhibitor alpha/metabolism
MH  - NF-kappa B/*metabolism
MH  - Nitric Oxide/metabolism
MH  - Nitric Oxide Synthase Type II/genetics/metabolism
MH  - Phosphorylation
MH  - Plant Extracts/isolation & purification/*pharmacology
MH  - *Potentilla/chemistry
MH  - RAW 264.7 Cells
MH  - Signal Transduction
MH  - Transcription Factor AP-1/*metabolism
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
OTO - NOTNLM
OT  - AP-1
OT  - NF-kappaB
OT  - Potentilla discolor
OT  - anti-inflammation
OT  - diarrhea
OT  - macrophage
EDAT- 2021/10/23 06:00
MHDA- 2022/01/27 06:00
CRDT- 2021/10/22 20:50
PHST- 2021/08/27 00:00 [received]
PHST- 2021/10/09 00:00 [revised]
PHST- 2021/10/13 00:00 [accepted]
PHST- 2021/10/23 06:00 [pubmed]
PHST- 2022/01/27 06:00 [medline]
PHST- 2021/10/22 20:50 [entrez]
AID - S0753-3322(21)01129-X [pii]
AID - 10.1016/j.biopha.2021.112345 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2021 Dec;144:112345. doi: 10.1016/j.biopha.2021.112345. Epub 
      2021 Oct 19.