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Tytuł pozycji:

Eurotium cristatum Fermented Loose Dark Tea Ameliorates Cigarette Smoke-Induced Lung Injury by MAPK Pathway and Enhances Hepatic Metabolic Detoxification by PXR / AhR Pathway in Mice.

Tytuł:
Eurotium cristatum Fermented Loose Dark Tea Ameliorates Cigarette Smoke-Induced Lung Injury by MAPK Pathway and Enhances Hepatic Metabolic Detoxification by PXR / AhR Pathway in Mice.
Autorzy:
Huang XX; Key Laboratory of Tea Science of Ministry of Education, National Research Center of Engineering Technology for Utilization of Functional Ingredients from Botanicals, College of Horticulture, Hunan Agricultural University, Changsha 410128, China.
Xu S; Key Laboratory of Tea Science of Ministry of Education, National Research Center of Engineering Technology for Utilization of Functional Ingredients from Botanicals, College of Horticulture, Hunan Agricultural University, Changsha 410128, China.
Yu LJ; Key Laboratory of Tea Science of Ministry of Education, National Research Center of Engineering Technology for Utilization of Functional Ingredients from Botanicals, College of Horticulture, Hunan Agricultural University, Changsha 410128, China.
Zhou YF; Key Laboratory of Tea Science of Ministry of Education, National Research Center of Engineering Technology for Utilization of Functional Ingredients from Botanicals, College of Horticulture, Hunan Agricultural University, Changsha 410128, China.
Zhou Y; Key Laboratory of Tea Science of Ministry of Education, National Research Center of Engineering Technology for Utilization of Functional Ingredients from Botanicals, College of Horticulture, Hunan Agricultural University, Changsha 410128, China.
Liu ZH; Key Laboratory of Tea Science of Ministry of Education, National Research Center of Engineering Technology for Utilization of Functional Ingredients from Botanicals, College of Horticulture, Hunan Agricultural University, Changsha 410128, China.; Hunan Provincial Key Laboratory for Germplasm Innovation and Utilization of Crop, Hunan Agricultural University, Changsha 410128, China.
Źródło:
Oxidative medicine and cellular longevity [Oxid Med Cell Longev] 2021 Mar 10; Vol. 2021, pp. 6635080. Date of Electronic Publication: 2021 Mar 10 (Print Publication: 2021).
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: 2011- : New York : Hindawi Pub. Corp.
Original Publication: 2008-2010: Austin, TX : Landes Bioscience
MeSH Terms:
Metabolic Detoxication, Phase I*
Aspergillus/*classification
Cigarette Smoking/*metabolism
Lung/*metabolism
Lung Injury/*drug therapy
MAP Kinase Signaling System/*drug effects
Plant Extracts/*pharmacology
Pregnane X Receptor/*metabolism
Receptors, Aryl Hydrocarbon/*metabolism
Signal Transduction/*drug effects
Animals ; Cigarette Smoking/pathology ; Female ; Lung/pathology ; Lung Injury/metabolism ; Mice ; Plant Extracts/chemistry
References:
Biochimie. 2019 Jan;156:47-58. (PMID: 30268700)
Brain Res. 2015 Nov 19;1627:90-100. (PMID: 26410779)
Mol Pharmacol. 2018 Feb;93(2):119-127. (PMID: 29113993)
World J Gastroenterol. 2006 Oct 14;12(38):6098-101. (PMID: 17036378)
Cardiovasc Res. 2011 Jun 1;90(3):475-83. (PMID: 21285293)
Int J Biol Macromol. 2018 Sep;116:120-127. (PMID: 29730012)
J Clin Diagn Res. 2013 Mar;7(3):580-8. (PMID: 23634430)
Nutrients. 2018 Dec 28;11(1):. (PMID: 30597920)
Am J Pathol. 2007 Mar;170(3):855-64. (PMID: 17322371)
Inflamm Res. 2020 Apr;69(4):423-434. (PMID: 32144443)
J Biochem Mol Toxicol. 2014 Oct;28(10):465-71. (PMID: 24957013)
Antioxid Redox Signal. 2017 Sep 1;27(7):433-451. (PMID: 28006950)
Free Radic Biol Med. 2015 Nov;88(Pt B):108-146. (PMID: 26122708)
Clin Appl Immunol Rev. 2006 Jan 1;6(1):53-72. (PMID: 23997664)
Food Chem Toxicol. 2014 Aug;70:120-7. (PMID: 24815822)
Clin Pharmacokinet. 1999 Jun;36(6):425-38. (PMID: 10427467)
Int J Chron Obstruct Pulmon Dis. 2015 Feb 02;10:261-76. (PMID: 25673984)
Gastroenterology. 2019 Sep;157(3):793-806.e14. (PMID: 31170413)
Oxid Med Cell Longev. 2018 Nov 8;2018:9364364. (PMID: 30533177)
J Nutr Biochem. 2017 Feb;40:1-13. (PMID: 27723473)
Eur Respir J. 2011 Nov;38(5):1019-28. (PMID: 21622588)
Pulm Pharmacol Ther. 2013 Oct;26(5):596-602. (PMID: 23499888)
Int J Mol Sci. 2018 Jul 23;19(7):. (PMID: 30041454)
Lancet Oncol. 2002 Aug;3(8):461-9. (PMID: 12147432)
Eur Respir J. 2013 Apr;41(4):966-73. (PMID: 22878872)
Free Radic Res. 2012 Sep;46(9):1123-9. (PMID: 22574903)
Tob Control. 2003 Dec;12(4):424-30. (PMID: 14660781)
Biosci Rep. 2020 Jan 31;40(1):. (PMID: 31894837)
J Allergy Clin Immunol. 2016 Jul;138(1):16-27. (PMID: 27373322)
Cell Biochem Funct. 2017 Jul;35(5):278-286. (PMID: 28749079)
iScience. 2018 Jun 29;4:44-63. (PMID: 30240752)
Phytomedicine. 2019 May;58:152768. (PMID: 31005721)
Food Funct. 2020 Apr 30;11(4):3516-3526. (PMID: 32253400)
Free Radic Biol Med. 2014 Apr;69:208-18. (PMID: 24486342)
J Biol Chem. 2008 Oct 24;283(43):28944-57. (PMID: 18697742)
Toxicol In Vitro. 2014 Mar;28(2):292-9. (PMID: 24269501)
J Ethnopharmacol. 2015 Dec 4;175:1-8. (PMID: 26342519)
Eur J Pharmacol. 2011 Mar 11;654(3):295-303. (PMID: 21238452)
Molecules. 2014 Nov 03;19(11):17839-47. (PMID: 25372398)
J Inflamm (Lond). 2007 Feb 14;4:3. (PMID: 17300721)
Food Sci Nutr. 2019 Dec 13;8(1):489-499. (PMID: 31993173)
J Food Sci. 2015 Apr;80(4):M809-17. (PMID: 25799937)
Antioxidants (Basel). 2019 Jul 10;8(7):. (PMID: 31295859)
Carcinogenesis. 2014 Jun;35(6):1228-37. (PMID: 24398671)
Chem Biol Interact. 2005 Jun 30;155(1-2):31-42. (PMID: 15970277)
Drug Metab Pharmacokinet. 2012;27(2):200-6. (PMID: 22076448)
J Biol Chem. 2011 Dec 16;286(50):43214-28. (PMID: 21984831)
Nutrients. 2015 Jul 01;7(7):5309-26. (PMID: 26140539)
Environ Health Perspect. 2020 Apr;128(4):47011. (PMID: 32352317)
Life Sci. 2020 Oct 15;259:118260. (PMID: 32795541)
Respir Res. 2017 Jul 24;18(1):142. (PMID: 28738859)
Chin J Integr Med. 2019 Oct;25(10):750-756. (PMID: 30588579)
Toxicol Sci. 2014 Jul;140(1):204-23. (PMID: 24752502)
Front Pharmacol. 2016 Nov 25;7:456. (PMID: 27932985)
Toxicol Sci. 2008 Jul;104(1):67-73. (PMID: 18381355)
Mol Nutr Food Res. 2018 Mar;62(6):e1700485. (PMID: 29345748)
Andrologia. 2018 Apr;50(3):. (PMID: 29164649)
Int J Mol Sci. 2015 Nov 02;16(11):26087-124. (PMID: 26540040)
Nat Rev Immunol. 2019 Mar;19(3):184-197. (PMID: 30718831)
Free Radic Res. 2019 May;53(5):486-496. (PMID: 31010354)
J Exp Clin Cancer Res. 2019 Jan 28;38(1):39. (PMID: 30691509)
Substance Nomenclature:
0 (Nr1i2 protein, mouse)
0 (Plant Extracts)
0 (Pregnane X Receptor)
0 (Receptors, Aryl Hydrocarbon)
SCR Organism:
Aspergillus cristatus
Entry Date(s):
Date Created: 20210329 Date Completed: 20210520 Latest Revision: 20210520
Update Code:
20240105
PubMed Central ID:
PMC7972846
DOI:
10.1155/2021/6635080
PMID:
33777316
Czasopismo naukowe
Cigarette smoke- (CS-) induced oxidative stress and inflammation in the lung are serious health problems. Primary and reprocessed tea products contain multiple antioxidants that have been reported to protect the lung against CS-induced injury. However, the beneficial effects of Eurotium cristatum fermented loose dark tea (ECT) and Eurotium cristatum particle metabolites (ECP) on CS-induced lung injury and its potential hepatic metabolic detoxification are still unclear. Therefore, sixty mice were randomly divided into six equal groups. CS-exposed mice were prevented or treated with ECP or ECT infusions for 12 or 8 weeks to determine the antioxidative stress, anti-inflammatory and potential metabolic detoxification of ECT and ECP. Thirty-six mice were randomly divided into six equal groups to observe the effects on hepatic metabolic detoxification by replacing daily drinking water with ECT. Results showed that CS significantly decreased the activities of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) and upregulated the expressions of malondialdehyde (MDA), tumor necrosis factor alpha (TNF- α ), interleukin-6 (IL-6), IL-8, and IL-1 β in serum. These adverse effects were modulated by ECP and ECT. In addition, ECT upregulated the mRNA expression of pregnane X receptor ( PXR ) and cytochrome P450 ( CYP450 ) in the liver on daily free drinking ECT mice group. Western blot analysis further revealed that in CS-exposed mice, ECP and ECT significantly decreased the phosphorylation of mitogen-activated protein kinase (MAPK) in the lung but upregulated the protein expressions of PXR and aryl hydrocarbon receptor ( AhR ) in the liver. Overall, our findings demonstrated that ECT and ECP protected against lung injury induced by CS via MAPK pathway and enhanced hepatic metabolic detoxification via PXR and AhR pathways. Therefore, daily intake of ECT and ECP can potentially protect against CS-induced oxidative and inflammatory injuries.
Competing Interests: The authors declare no conflict of interest.
(Copyright © 2021 Xiang-Xiang Huang et al.)

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