PMID- 27260408
OWN - NLM
STAT- MEDLINE
DCOM- 20170418
LR  - 20171116
IS  - 1872-7573 (Electronic)
IS  - 0378-8741 (Linking)
VI  - 190
DP  - 2016 Aug 22
TI  - Juniperus rigida Sieb. extract inhibits inflammatory responses via attenuation of 
      TRIF-dependent signaling and inflammasome activation.
PG  - 91-9
LID - S0378-8741(16)30341-5 [pii]
LID - 10.1016/j.jep.2016.05.059 [doi]
AB  - ETHNOPHARMACOLOGICAL RELEVANCE: Juniperus rigida Sieb. (J. rigida) is used for 
      medicinal purposes in Asian countries to treat inflammation-related disorders, 
      such as neuralgia, dropsy, and gout. AIM OF THE STUDY: The anti-inflammatory 
      effects of J. rigida extract (JR) and its underlying mechanisms were explored 
      both in in vitro cell lines and in vivo metabolic disease models. MATERIAL AND 
      METHODS: Lipopolysaccharide (LPS)-stimulated RAW264.7 murine macrophages were 
      used to study the changes in inflammatory responses in vitro. Bone marrow-derived 
      macrophages (BMDMs) were used to study the regulatory effect of JR on 
      inflammasome activation. The murine model for monosodium urate (MSU)-induced 
      peritonitis and high-fat diet (HFD)-induced type 2 diabetes were employed to 
      study the effect of JR on in vivo efficacy. RESULTS: JR suppressed the 
      MSU-induced in vivo inflammatory response by attenuation of proinflammatory 
      cytokines, including interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha 
      (TNF-alpha). In the in vitro study, JR suppressed IL-1beta secretion via regulation of 
      apoptosis-associated speck-like protein containing a CARD (ASC) oligomerization, 
      leading to the inhibition of inflammasome activation. JR also inhibited the 
      LPS-stimulated release of proinflammatory mediators, such as nitric oxide (NO), 
      TNF-alpha, and IL-6 in RAW264.7 cells. The inhibitory effects of JR were mediated 
      through the regulation of the TRIF-dependent signaling pathway from JAK1/STAT1 
      phosphorylation. Furthermore, JR showed inhibitory effects on HFD-induced type 2 
      diabetes in a mouse model through the regulation of blood glucose and serum 
      IL-1beta. CONCLUSIONS: Our results indicate that JR attenuates both LPS-stimulated 
      and danger-signal-induced inflammatory responses in macrophages via regulation of 
      the key inflammatory mechanisms, providing scientific support for its traditional 
      use in the treatment of various inflammation-related metabolic disorders.
CI  - Copyright (c) 2016 Elsevier Ireland Ltd. All rights reserved.
FAU - Han, Ji-Won
AU  - Han JW
AD  - Department of Biotechnology, College of Biomedical & Health Science, Research 
      Institute of Inflammatory Diseases, Konkuk University, Chungju, South Korea.
FAU - Shim, Do-Wan
AU  - Shim DW
AD  - Department of Biotechnology, College of Biomedical & Health Science, Research 
      Institute of Inflammatory Diseases, Konkuk University, Chungju, South Korea.
FAU - Shin, Woo-Young
AU  - Shin WY
AD  - Department of Biotechnology, College of Biomedical & Health Science, Research 
      Institute of Inflammatory Diseases, Konkuk University, Chungju, South Korea.
FAU - Kim, Myong-Ki
AU  - Kim MK
AD  - Department of Food Science and Engineering, Seowon University, Cheongju, South 
      Korea.
FAU - Shim, Eun-Jeong
AU  - Shim EJ
AD  - Department of Biotechnology, College of Biomedical & Health Science, Research 
      Institute of Inflammatory Diseases, Konkuk University, Chungju, South Korea.
FAU - Sun, Xiao
AU  - Sun X
AD  - Department of Biotechnology, College of Biomedical & Health Science, Research 
      Institute of Inflammatory Diseases, Konkuk University, Chungju, South Korea.
FAU - Koppula, Sushruta
AU  - Koppula S
AD  - Department of Biotechnology, College of Biomedical & Health Science, Research 
      Institute of Inflammatory Diseases, Konkuk University, Chungju, South Korea.
FAU - Kim, Tack-Joong
AU  - Kim TJ
AD  - Division of Biological Science and Technology, Institute of Biomaterials, Yonsei 
      University, Wonju, South Korea.
FAU - Kang, Tae-Bong
AU  - Kang TB
AD  - Department of Biotechnology, College of Biomedical & Health Science, Research 
      Institute of Inflammatory Diseases, Konkuk University, Chungju, South Korea.
FAU - Lee, Kwang-Ho
AU  - Lee KH
AD  - Department of Biotechnology, College of Biomedical & Health Science, Research 
      Institute of Inflammatory Diseases, Konkuk University, Chungju, South Korea. 
      Electronic address: kwangho@kku.ac.kr.
LA  - eng
PT  - Journal Article
DEP - 20160531
PL  - Ireland
TA  - J Ethnopharmacol
JT  - Journal of ethnopharmacology
JID - 7903310
RN  - 0 (Adaptor Proteins, Vesicular Transport)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (Blood Glucose)
RN  - 0 (CARD Signaling Adaptor Proteins)
RN  - 0 (Cytokines)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Inflammasomes)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
RN  - 0 (Nlrp3 protein, mouse)
RN  - 0 (Plant Extracts)
RN  - 0 (Pycard protein, mouse)
RN  - 0 (STAT1 Transcription Factor)
RN  - 0 (Stat1 protein, mouse)
RN  - 0 (TICAM-1 protein, mouse)
RN  - 268B43MJ25 (Uric Acid)
RN  - EC 2.7.10.2 (Jak1 protein, mouse)
RN  - EC 2.7.10.2 (Janus Kinase 1)
SB  - IM
MH  - Adaptor Proteins, Vesicular Transport/*metabolism
MH  - Animals
MH  - Anti-Inflammatory Agents/isolation & purification/*pharmacology
MH  - Apoptosis Regulatory Proteins/metabolism
MH  - Blood Glucose/drug effects/metabolism
MH  - CARD Signaling Adaptor Proteins
MH  - Chromatography, High Pressure Liquid
MH  - Cytokines/metabolism
MH  - Diabetes Mellitus, Experimental/immunology/metabolism/*prevention & control
MH  - Diabetes Mellitus, Type 2/immunology/metabolism/*prevention & control
MH  - Diet, High-Fat
MH  - Dose-Response Relationship, Drug
MH  - Female
MH  - Hypoglycemic Agents/isolation & purification/*pharmacology
MH  - Inflammasomes/*drug effects/immunology/metabolism
MH  - Inflammation/immunology/metabolism/*prevention & control
MH  - Inflammation Mediators/metabolism
MH  - Janus Kinase 1/metabolism
MH  - Juniperus/*chemistry
MH  - Lipopolysaccharides/pharmacology
MH  - Macrophages/*drug effects/immunology/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
MH  - Peritonitis/chemically induced/immunology/metabolism/*prevention & control
MH  - Phosphorylation
MH  - Phytotherapy
MH  - Plant Extracts/isolation & purification/*pharmacology
MH  - Plants, Medicinal
MH  - RAW 264.7 Cells
MH  - STAT1 Transcription Factor/metabolism
MH  - Signal Transduction/*drug effects
MH  - Uric Acid
OTO - NOTNLM
OT  - ASC
OT  - IL-1beta
OT  - Inflammasome
OT  - Juniperus rigida
OT  - TRIF
OT  - Type-II diabetes
EDAT- 2016/06/05 06:00
MHDA- 2017/04/19 06:00
CRDT- 2016/06/05 06:00
PHST- 2016/01/28 00:00 [received]
PHST- 2016/04/19 00:00 [revised]
PHST- 2016/05/29 00:00 [accepted]
PHST- 2016/06/05 06:00 [entrez]
PHST- 2016/06/05 06:00 [pubmed]
PHST- 2017/04/19 06:00 [medline]
AID - S0378-8741(16)30341-5 [pii]
AID - 10.1016/j.jep.2016.05.059 [doi]
PST - ppublish
SO  - J Ethnopharmacol. 2016 Aug 22;190:91-9. doi: 10.1016/j.jep.2016.05.059. Epub 2016 
      May 31.