Informacja

Drogi użytkowniku, aplikacja do prawidłowego działania wymaga obsługi JavaScript. Proszę włącz obsługę JavaScript w Twojej przeglądarce.

Przeglądasz jako GOŚĆ
Tytuł pozycji:

Cordycepin Attenuates IFN-γ-Induced Macrophage IP-10 and Mig Expressions by Inhibiting STAT1 Activity in CFA-Induced Inflammation Mice Model.

Tytuł :
Cordycepin Attenuates IFN-γ-Induced Macrophage IP-10 and Mig Expressions by Inhibiting STAT1 Activity in CFA-Induced Inflammation Mice Model.
Autorzy :
Yang R; Department of Immunology, School of Preclinical Medicine, Center for Genomic and Personalized Medicine, Guangxi Medical University, 22 Shuangyong Road, Nanning, Guangxi, 530021, People's Republic of China. .
Wang X; Department of Immunology, School of Preclinical Medicine, Center for Genomic and Personalized Medicine, Guangxi Medical University, 22 Shuangyong Road, Nanning, Guangxi, 530021, People's Republic of China.
Xi D; Department of Immunology, School of Preclinical Medicine, Center for Genomic and Personalized Medicine, Guangxi Medical University, 22 Shuangyong Road, Nanning, Guangxi, 530021, People's Republic of China.
Mo J; Department of Immunology, School of Preclinical Medicine, Center for Genomic and Personalized Medicine, Guangxi Medical University, 22 Shuangyong Road, Nanning, Guangxi, 530021, People's Republic of China.
Wang K; Department of Physiology, School of Preclinical Medicine, Guangxi Medical University, 22 Shuangyong Road, Nanning, Guangxi, 530021, People's Republic of China.
Luo S; Department of Immunology, School of Preclinical Medicine, Center for Genomic and Personalized Medicine, Guangxi Medical University, 22 Shuangyong Road, Nanning, Guangxi, 530021, People's Republic of China.
Wei J; Department of Physiology, School of Preclinical Medicine, Guangxi Medical University, 22 Shuangyong Road, Nanning, Guangxi, 530021, People's Republic of China.
Ren Z; State Key Laboratory of Biocontrol, Guangdong Province Key Laboratory of Pharmaceutical Functional Genes, National Engineering Research Center of South China Sea Marine Biotechnology, Department of Biochemistry, College of Life Sciences, Sun Yat-sen University, Guangzhou, 510275, People's Republic of China.
Pang H; Department of Physiology, School of Preclinical Medicine, Guangxi Medical University, 22 Shuangyong Road, Nanning, Guangxi, 530021, People's Republic of China.
Luo Y; Department of Clinical Laboratory, Peoples's Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi, 530021, People's Republic of China. .
Pokaż więcej
Źródło :
Inflammation [Inflammation] 2020 Apr; Vol. 43 (2), pp. 752-764.
Typ publikacji :
Journal Article
Język :
English
Imprint Name(s) :
Publication: 1999- : New York, NY : Kluwer Academic/Plenum Publishers
Original Publication: New York, Plenum Press.
MeSH Terms :
Chemokine CXCL10/*antagonists & inhibitors
Chemokine CXCL9/*antagonists & inhibitors
Deoxyadenosines/*therapeutic use
Interferon-gamma/*toxicity
Macrophages/*drug effects
STAT1 Transcription Factor/*antagonists & inhibitors
Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Chemokine CXCL10/biosynthesis ; Chemokine CXCL9/biosynthesis ; Deoxyadenosines/pharmacology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Female ; Freund's Adjuvant/toxicity ; Gene Expression ; Inflammation/chemically induced ; Inflammation/drug therapy ; Inflammation/metabolism ; Macrophages/metabolism ; Mice ; RAW 264.7 Cells ; Random Allocation ; STAT1 Transcription Factor/metabolism
References :
Oncotarget. 2017 Oct 4;8(55):93712-93728. (PMID: 29212184)
Int Immunopharmacol. 2018 Jul;60:18-25. (PMID: 29702279)
Eur J Pharmacol. 2018 Jan 5;818:110-114. (PMID: 29054740)
J Immunol. 2015 Dec 15;195(12):5657-66. (PMID: 26573836)
PeerJ. 2016 May 10;4:e1992. (PMID: 27190710)
BMC Gastroenterol. 2016 Jan 16;16:7. (PMID: 26772979)
J Immunol. 2011 Feb 1;186(3):1685-93. (PMID: 21178011)
Diabetes Care. 2010 Jul;33(7):1686-7. (PMID: 20587729)
J Immunol. 2006 Dec 1;177(11):8072-9. (PMID: 17114481)
Front Immunol. 2014 Oct 07;5:491. (PMID: 25339958)
Biosci Biotechnol Biochem. 2004 Nov;68(11):2257-64. (PMID: 15564662)
Am J Physiol Gastrointest Liver Physiol. 2004 Nov;287(5):G1044-52. (PMID: 15246962)
Biochem Biophys Res Commun. 2018 Sep 18;503(4):2666-2672. (PMID: 30086883)
Antimicrob Agents Chemother. 1998 Jun;42(6):1424-7. (PMID: 9624488)
Evid Based Complement Alternat Med. 2017;2017:8246420. (PMID: 29104606)
Mediators Inflamm. 2017;2017:3946706. (PMID: 28522898)
Biochemistry. 1991 Feb 26;30(8):2027-33. (PMID: 1705437)
Nature. 1995 Apr 13;374(6523):647-50. (PMID: 7715705)
Int Immunopharmacol. 2012 Dec;14(4):698-703. (PMID: 23102662)
J Cell Sci. 2004 Mar 15;117(Pt 8):1281-3. (PMID: 15020666)
Immunol Rev. 2015 Mar;264(1):182-203. (PMID: 25703560)
Patol Fiziol Eksp Ter. 2015 Apr-Jun;59(2):99-111. (PMID: 26571814)
Immune Netw. 2009 Dec;9(6):255-64. (PMID: 20157613)
Evid Based Complement Alternat Med. 2017;2017:1960517. (PMID: 29238384)
Toxins (Basel). 2012 Sep;4(9):676-94. (PMID: 23105975)
J Pain Res. 2017 Jul 27;10:1777-1786. (PMID: 28794657)
Arthritis Rheum. 2012 Dec;64(12):3856-66. (PMID: 22941906)
Indian J Exp Biol. 2015 Jan;53(1):36-43. (PMID: 25675710)
Res Immunol. 1998 Sep-Oct;149(7-8):685-8. (PMID: 9851524)
Int J Oncol. 2014 Jul;45(1):209-18. (PMID: 24789042)
Inflammation. 2014 Aug;37(4):1044-9. (PMID: 24493324)
Clin Exp Metastasis. 2002;19(4):351-8. (PMID: 12090476)
J Exp Med. 1998 Jun 15;187(12):2103-8. (PMID: 9625771)
Drug Des Devel Ther. 2014 Oct 16;8:1941-53. (PMID: 25342887)
Inflammation. 2015;38(3):1036-43. (PMID: 25417131)
Immunobiology. 2015 Sep;220(9):1067-74. (PMID: 26003840)
Mol Immunol. 2015 Dec;68(2 Pt C):597-605. (PMID: 26514428)
Nature. 1950 Dec 2;166(4231):949. (PMID: 14796634)
Cell. 2010 Mar 19;140(6):771-6. (PMID: 20303867)
Grant Information :
2018GXNSFAA281211 Natural Science Foundation of Guangxi Province; 81360312 National Natural Science Foundation of China; 81402306 National Natural Science Foundation of China
Contributed Indexing :
Keywords: IFN-γ; IP-10; cordycepin; macrophage; mig
Substance Nomenclature :
0 (Antineoplastic Agents)
0 (Chemokine CXCL10)
0 (Chemokine CXCL9)
0 (Cxcl10 protein, mouse)
0 (Cxcl9 protein, mouse)
0 (Deoxyadenosines)
0 (STAT1 Transcription Factor)
0 (Stat1 protein, mouse)
82115-62-6 (Interferon-gamma)
9007-81-2 (Freund's Adjuvant)
GZ8VF4M2J8 (cordycepin)
Entry Date(s) :
Date Created: 20191225 Date Completed: 20210208 Latest Revision: 20210208
Update Code :
20210211
DOI :
10.1007/s10753-019-01162-3
PMID :
31873836
Czasopismo naukowe
Cordycepin, a natural derivative of adenosine, has been shown to exert pharmacological properties including anti-oxidation, antitumor, and immune regulation. It is reported that cordycepin is involved in the regulation of macrophage function. However, the effect of cordycepin on inflammatory cell infiltration in inflammation remains ambiguous. In this study, we investigated the potential role of cordycepin playing in macrophage function in CFA-induced inflammation mice model. In this model, we found that cordycepin prevented against macrophage infiltration in paw tissue and reduced interferon-γ (IFN-γ) production in both serum and paw tissue. Using luciferase reporter assay, we found that cordycepin suppressed IFN-γ-induced activators of transcription-1 (STAT1) transcriptional activity in a dose-dependent manner. Moreover, western blotting data demonstrated that cordycepin inhibited IFN-γ-induced STAT1 activation through attenuating STAT1 phosphorylation. Further investigations revealed that cordycepin inhibited the expressions of IFN-γ-inducible protein 10 (IP-10) and monokine induced by IFN-γ (Mig), which were the effector genes in IFN-γ-induced STAT1 signaling. Meanwhile, the excessive inflammatory cell infiltration in paw tissue was reduced by cordycepin. These findings demonstrate that cordycepin alleviates excessive inflammatory cell infiltration through down-regulation of macrophage IP-10 and Mig expressions via suppressing STAT1 phosphorylation. Thus, cordycepin may be a potential therapeutic approach to prevent and treat inflammation-associated diseases.

Ta witryna wykorzystuje pliki cookies do przechowywania informacji na Twoim komputerze. Pliki cookies stosujemy w celu świadczenia usług na najwyższym poziomie, w tym w sposób dostosowany do indywidualnych potrzeb. Korzystanie z witryny bez zmiany ustawień dotyczących cookies oznacza, że będą one zamieszczane w Twoim komputerze. W każdym momencie możesz dokonać zmiany ustawień dotyczących cookies