Antagonistic Effects Of Baicalin On
Mycoplasma gallisepticum
baicalin
energy metabolism
inflammation
lungs
Journal
Infection and drug resistance
ISSN: 1178-6973
Titre abrégé: Infect Drug Resist
Pays: New Zealand
ID NLM: 101550216
Informations de publication
Date de publication:
2019
2019
Historique:
received:
13
07
2019
accepted:
13
09
2019
entrez:
22
10
2019
pubmed:
22
10
2019
medline:
22
10
2019
Statut:
epublish
Résumé
Baicalin possesses potential anti-inflammatory, anti-tumor and anti-oxidant activities. In the present study, we attempted to investigate the preventive effects of baicalin against Experimental chickens were randomly divided into 1) control group, 2) MG infection group, 3) MG-infected group treated with baicalin at a dose of 450 mg/kg and 4) baicalin alone treated group (450 mg/kg). After 7 days of post-treatment, serum and lung tissues were collected for different experimental analyses. The hallmarks of inflammation, apoptosis and energy metabolism dysfunction were detected by histological and ultrastructural examination, qRT-PCR, Western blotting and terminal deoxynucleotidyl transferase-mediated dUTP nick endlabeling (TUNEL) assay. The level of serum inflammatory markers were increased with MG infection. Histological and ultrastructural analysis showed excessive inflammatory cells infiltrates, alveolar wall thickening, hemorrhages, mitochondrial and nuclear damage, including mitochondrial swelling and condensation of DNA in the lungs of chickens infected with MG. TUNEL assay positive-stained nuclei were significantly increased in MG infection group. In addition, the mRNA and protein expression level of energy metabolism-related genes and ATPase activities were significantly reduced. Meanwhile, MG-induced morphological and ultrastructural changes were partially disappeared with baicalin-treatment, and the level of serum inflammatory markers were significantly reduced. It has been noted that baicalin significantly attenuated MG-induced inflammation and apoptosis in the chicken lungs through the suppression of nuclear factor-kappa B and reduced extensive positive-stained apoptotic nuclei. More importantly, ATPase activities and mRNA and protein expression level of energy metabolism-related genes were significantly improved with baicalin-treatment in the lungs of chickens infected with MG. Conclusively, it has been suggested from these results that baicalin-treatment efficiently prevented MG-induced inflammation, apoptosis and energy metabolism dysfunction in the chicken lungs and provide basis for new therapeutic targets to control MG infection.
Sections du résumé
BACKGROUND
BACKGROUND
Baicalin possesses potential anti-inflammatory, anti-tumor and anti-oxidant activities. In the present study, we attempted to investigate the preventive effects of baicalin against
METHODS
METHODS
Experimental chickens were randomly divided into 1) control group, 2) MG infection group, 3) MG-infected group treated with baicalin at a dose of 450 mg/kg and 4) baicalin alone treated group (450 mg/kg). After 7 days of post-treatment, serum and lung tissues were collected for different experimental analyses. The hallmarks of inflammation, apoptosis and energy metabolism dysfunction were detected by histological and ultrastructural examination, qRT-PCR, Western blotting and terminal deoxynucleotidyl transferase-mediated dUTP nick endlabeling (TUNEL) assay.
RESULTS
RESULTS
The level of serum inflammatory markers were increased with MG infection. Histological and ultrastructural analysis showed excessive inflammatory cells infiltrates, alveolar wall thickening, hemorrhages, mitochondrial and nuclear damage, including mitochondrial swelling and condensation of DNA in the lungs of chickens infected with MG. TUNEL assay positive-stained nuclei were significantly increased in MG infection group. In addition, the mRNA and protein expression level of energy metabolism-related genes and ATPase activities were significantly reduced. Meanwhile, MG-induced morphological and ultrastructural changes were partially disappeared with baicalin-treatment, and the level of serum inflammatory markers were significantly reduced. It has been noted that baicalin significantly attenuated MG-induced inflammation and apoptosis in the chicken lungs through the suppression of nuclear factor-kappa B and reduced extensive positive-stained apoptotic nuclei. More importantly, ATPase activities and mRNA and protein expression level of energy metabolism-related genes were significantly improved with baicalin-treatment in the lungs of chickens infected with MG.
CONCLUSION
CONCLUSIONS
Conclusively, it has been suggested from these results that baicalin-treatment efficiently prevented MG-induced inflammation, apoptosis and energy metabolism dysfunction in the chicken lungs and provide basis for new therapeutic targets to control MG infection.
Identifiants
pubmed: 31632098
doi: 10.2147/IDR.S223085
pii: 223085
pmc: PMC6781171
doi:
Types de publication
Journal Article
Langues
eng
Pagination
3075-3089Informations de copyright
© 2019 Ishfaq et al.
Déclaration de conflit d'intérêts
All the authors have no potential conflicts of interests regarding the publication of this manuscript.
Références
Avian Pathol. 1997;26(2):391-8
pubmed: 18483915
Vaccine. 2007 Dec 12;25(51):8611-21
pubmed: 18006123
Avian Pathol. 2012;41(1):51-7
pubmed: 22845321
Cell. 2008 Sep 5;134(5):703-7
pubmed: 18775299
Microbes Infect. 2009 May-Jun;11(6-7):671-9
pubmed: 19379824
Nat Rev Immunol. 2011 Feb;11(2):81
pubmed: 21469396
Microbiol Mol Biol Rev. 1998 Dec;62(4):1094-156
pubmed: 9841667
Cancer Cell Int. 2016 Feb 16;16:9
pubmed: 26884725
Avian Dis. 1996 Apr-Jun;40(2):480-3
pubmed: 8790904
Isr J Med Sci. 1984 Oct;20(10):982-4
pubmed: 6511325
Sci Rep. 2018 Jan 16;8(1):807
pubmed: 29339754
Int Immunopharmacol. 2013 Feb;15(2):450-6
pubmed: 23261363
Oncotarget. 2017 Mar 28;8(13):20695-20705
pubmed: 28157700
Front Pharmacol. 2017 Aug 18;8:547
pubmed: 28868036
Am J Vet Res. 1979 Jul;40(7):1009-14
pubmed: 507485
Biol Trace Elem Res. 2018 Dec;186(2):521-528
pubmed: 29679350
Trends Microbiol. 1999 Dec;7(12):493-9
pubmed: 10603485
Eur J Med Chem. 2017 Jan 27;126:844-852
pubmed: 27960146
Curr Opin Immunol. 2000 Apr;12(2):215-8
pubmed: 10712949
Microbiology. 2000 May;146 ( Pt 5):1223-9
pubmed: 10832650
Vet Microbiol. 2017 Nov;211:112-118
pubmed: 29102105
Infect Immun. 2002 Dec;70(12):6839-45
pubmed: 12438360
Nat Rev Microbiol. 2005 Apr;3(4):281-94
pubmed: 15806094
Vet Rec. 2005 Apr 16;156(16):513-5
pubmed: 15833969
Immunology. 2004 Sep;113(1):121-9
pubmed: 15312143
Neurotoxicol Teratol. 2016 May-Jun;55:32-7
pubmed: 27018023
Immunol Cell Biol. 1998 Dec;76(6):526-34
pubmed: 9893030
Int J Mol Sci. 2012 Dec 20;14(1):146-57
pubmed: 23344025
Physiol Rev. 2003 Apr;83(2):417-32
pubmed: 12663864
J Immunol. 2005 Oct 1;175(7):4641-6
pubmed: 16177110
Exp Ther Med. 2013 Jan;5(1):338-342
pubmed: 23251295
Methods. 2001 Dec;25(4):402-8
pubmed: 11846609
Poult Sci. 2019 Aug 03;:null
pubmed: 31376349
Nature. 2013 Jan 17;493(7432):346-55
pubmed: 23325217
Nat Rev Microbiol. 2010 Jun;8(6):401-12
pubmed: 20453875
Environ Toxicol Pharmacol. 2018 Apr;59:94-104
pubmed: 29550706
Infect Immun. 2005 Sep;73(9):5410-9
pubmed: 16113257
Front Pharmacol. 2018 May 25;9:554
pubmed: 29887802
Poult Sci. 2015 Jul;94(7):1483-92
pubmed: 25910901
Am J Vet Res. 1985 Jan;46(1):116-22
pubmed: 3970413
Sci Total Environ. 2019 Apr 1;659:354-362
pubmed: 30599354
Infect Immun. 2015 Nov 02;84(1):266-74
pubmed: 26527215
Front Cell Infect Microbiol. 2013 Jul 09;3:24
pubmed: 23847769
Pharmacol Res. 2015 Oct;100:296-308
pubmed: 26318266
Mol Cell. 2013 Feb 7;49(3):399-410
pubmed: 23395270
Infect Immun. 2015 Nov 09;84(1):351-5
pubmed: 26553465
Mol Immunol. 2017 Jul;87:161-170
pubmed: 28478286
Front Pharmacol. 2017 Mar 21;8:143
pubmed: 28377720