Differential Expression of CD3, TNF-α, and VEGF Induced by Olanzapine on the Spleen of Adult Male Albino Rats and the Possible Protective Role of Vitamin C.
CD3
TNF-α
VEGF
olanzapine
spleen
vitamin C
Journal
Biomedicines
ISSN: 2227-9059
Titre abrégé: Biomedicines
Pays: Switzerland
ID NLM: 101691304
Informations de publication
Date de publication:
23 May 2019
23 May 2019
Historique:
received:
14
04
2019
revised:
13
05
2019
accepted:
21
05
2019
entrez:
26
5
2019
pubmed:
28
5
2019
medline:
28
5
2019
Statut:
epublish
Résumé
Olanzapine is an antipsychotic drug effective in the treatment of stress-associated psychiatric illnesses, but its effect on the spleen remains unclear. Vitamin C is essential for the optimum function of the immune system. We aim to investigate the effect of Olanzapine on spleen structures and to assess the protective effect of vitamin C. Forty adult male albino rats were divided into four groups: group (I), a control; group (II), rats were given vitamin C at 40 mg/kg body weight; group (III), rats were given Olanzapine at 2 mg/kg body weight; and group (IV), rats were given vitamin C and Olanzapine at the same dose of group (II) and group (III) for one month. The hematoxylin and eosin (H&E) of the olanzapine treated group showed focal areas of cellular depletion and a decrease in the size of the white pulp. The red pulp was expanded and showed marked congestion and dilatation of blood sinusoids. Cluster of differentiation 3 (CD3) was significantly reduced, however both tumor necrosis factor alpha (TNF-α), and vascular endothelial growth factor (VEGF) were significantly higher. The administration of vitamin C repaired structural and immunohistochemical changes via increased CD3 and decreased TNF-α and VEGF. Therefore, the oxidative and the inflammatory pathways may be the possible mechanisms underlying olanzapine immunotoxicity. Vitamin C exerted immune modulator and antioxidant effects against olanzapine.
Identifiants
pubmed: 31126077
pii: biomedicines7020039
doi: 10.3390/biomedicines7020039
pmc: PMC6631609
pii:
doi:
Types de publication
Journal Article
Langues
eng
Références
Pol J Pharmacol. 2002 Nov-Dec;54(6):737-42
pubmed: 12866735
Ann Nutr Metab. 2006;50(2):85-94
pubmed: 16373990
Neuropsychopharmacology. 2007 Feb;32(2):289-97
pubmed: 17035934
Toxicol Pathol. 2006;34(5):455-65
pubmed: 17067939
Behav Pharmacol. 2007 Sep;18(5-6):391-418
pubmed: 17762509
Int J Neuropsychopharmacol. 2008 Dec;11(8):1097-104
pubmed: 18466668
J Psychopharmacol. 2010 Oct;24(10):1499-504
pubmed: 19282419
Br J Pharmacol. 2009 Aug;157(7):1097-110
pubmed: 19508394
Eur J Pharmacol. 2010 May 25;634(1-3):170-7
pubmed: 20176014
Brain Res. 2010 Sep 2;1350:167-75
pubmed: 20570665
Behav Brain Res. 2011 Mar 1;217(2):337-46
pubmed: 21056063
Inflamm Allergy Drug Targets. 2011 Feb;10(1):54-63
pubmed: 21184650
Neuropeptides. 2012 Feb;46(1):1-10
pubmed: 21719103
J Biomed Mater Res A. 2012 Apr;100(4):894-902
pubmed: 22275130
Antioxid Redox Signal. 2013 Dec 10;19(17):2054-67
pubmed: 23249337
Rev Esp Enferm Dig. 2012 Dec;104(11):617-8
pubmed: 23368661
Cell Immunol. 2013 Jul-Aug;284(1-2):104-10
pubmed: 23973873
J Psychopharmacol. 2014 Dec;28(12):1161-9
pubmed: 25336715
Int J Nanomedicine. 2015 Feb 16;10:1335-57
pubmed: 25733828
Xenobiotica. 2016;46(4):369-78
pubmed: 26364812
Eur J Pharm Sci. 2016 Jan 1;81:94-102
pubmed: 26474692
J Immunotoxicol. 2016 May;13(3):349-54
pubmed: 26492975
J Psychiatr Res. 2016 May;76:59-65
pubmed: 26894301
Exp Ther Med. 2017 Feb;13(2):723-730
pubmed: 28352358
Indian J Psychol Med. 2017 Jul-Aug;39(4):537-538
pubmed: 28852258
FEBS Lett. 2018 Mar;592(5):692-702
pubmed: 29292494
Toxicol Ind Health. 2019 Jan;35(1):43-52
pubmed: 30463494
Free Radic Biol Med. 1997;22(1-2):287-305
pubmed: 8958154