The protective effects of trimetazidine against ovary ischemia-reperfusion injury via the TLR4/Nf-kB signal pathway.
inflammation
ischemia-reperfusion
ovary
oxidative stress
rat
trimetazidine
Journal
Journal of biochemical and molecular toxicology
ISSN: 1099-0461
Titre abrégé: J Biochem Mol Toxicol
Pays: United States
ID NLM: 9717231
Informations de publication
Date de publication:
Aug 2022
Aug 2022
Historique:
revised:
12
04
2022
received:
25
01
2022
accepted:
18
05
2022
pubmed:
29
5
2022
medline:
17
8
2022
entrez:
28
5
2022
Statut:
ppublish
Résumé
Late diagnosis and treatment of ovarian ischemia can lead to worsening of ischemia, irreversible damage to ovarian functions and infertility. In this process, there is no approved medical treatment that can reduce the negative effects of ischemia and contribute positively to ovarian functions during reperfusion after detorsion. Rats were randomly assigned into one of six groups of eight animals each. The groups were designed as follows: The control group, The ischemia(I) group, The Ischemia + Trimetazidine (I + TMZ) (20 mg/kg) group, and The ischemia-reperfusion group (I/R). The Ischemia-Reperfusion + Trimetazidine (I/R + TMZ) (20 mg/kg) group, and The Sham + Trimetazidine (Sham + TMZ) (20 mg/kg) group. In this study performed thiobarbituric acid reactive substances (TBARS), total thiol (-SH), interleukin 1 beta (IL-1β), interleukin 6 (IL-6), toll-like receptor 4 (TLR4), and nuclear factor-kappa B(NF-κβ). Increased oxidative stress and inflammation were as a result of ovarian I and I/R application. Trimetazidine (TMZ), was sufficient to reduce the oxidative stress and inflammation. TLR4 and NF-κβ, which were upregulated by oxidative stress and inflammation, were regressed by TMZ. TMZ should be considered as a potential therapeutic agent in addition to surgery in the clinical treatment of ovarian torsion.
Substances chimiques
NF-kappa B
0
Tlr4 protein, rat
0
Toll-Like Receptor 4
0
Trimetazidine
N9A0A0R9S8
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e23114Informations de copyright
© 2022 Wiley Periodicals LLC.
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