Investigation of effect of nintedanib in experimental uveitis model.
Interleukin-6
Nintedanib
Tumour necrosis factor-α
Uveitis
Journal
Cutaneous and ocular toxicology
ISSN: 1556-9535
Titre abrégé: Cutan Ocul Toxicol
Pays: England
ID NLM: 101266892
Informations de publication
Date de publication:
Mar 2022
Mar 2022
Historique:
pubmed:
16
12
2021
medline:
27
5
2022
entrez:
15
12
2021
Statut:
ppublish
Résumé
This study aims to investigate the protective efficacy of nintedanib in experimental uveitis induced by endotoxins. In this study, 24 Wistar albino rats were randomly divided into three groups: Group I was the healthy control with no uveitis that did not receive any treatment, Group II (sham) group did not receive treatment, and Group III (nintedanib) received oral nintedanib for 10 days. On the 10th day, endotoxin-induced uveitis (EIU) was induced by lipopolysaccharide (LPS) injection in Groups II and III. The clinical activity score was evaluated in all groups at the 24th hour, when uveitis formation was thought to be the most intense after LPS injection. All rats were then killed via anaesthesia. Tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) levels were measured in their right eyes using the enzyme-linked immunosorbent assay (ELISA) method. Further, histopathological examinations were performed on their left eyes. For Groups I, II, and III, the IL-6 levels were 30.88 ± 1.79, 36.77 ± 1.21, and 30.93 ± 3.96 mg/pr, respectively, and TNF-α levels were 50.20 ± 3.24, 59.87 ± 2.98, and 50.23 ± 4.83 mg/pr, respectively. IL-6, TNF-α levels and clinical activity score were higher in the sham group compared to the other groups, and it decreased significantly in the treatment group ( Nintedanib may be preferable as a new agent for treating non-infectious uveitis. However, further studies are needed to evaluate its long-term effects, effects on other antiinflammatory pathways, side-effects, and ideal dose optimization.
Identifiants
pubmed: 34905992
doi: 10.1080/15569527.2021.2016804
doi:
Substances chimiques
Indoles
0
Interleukin-6
0
Lipopolysaccharides
0
Tumor Necrosis Factor-alpha
0
nintedanib
G6HRD2P839
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM