The influencer effect of Dexmedetomidine on radioiodine relevant to lacrimal gland impairment.
Int Ophthalmol
; 44(1): 115, 2024 Feb 27.
Article
em En
| MEDLINE
| ID: mdl-38411703
ABSTRACT
PURPOSE:
To assess the potential influencing effects of Dexmedetomidine on impaired lacrimal glands after high-dose radioiodine treatment (RAI).METHODS:
Thirty-six rats were arbitrarily separated into 3 groups Sham, RAI, and Dexmedetomidine. Dexmedetomidine group was given Dexmedetomidine and RAI, the Sham group was given the same millimeters of saline, and the RAI group was given RAI only. All forms of lacrimal glands, including harderian glands (HG), extraorbital (EG), and intraorbital (IG) lacrimal glands, were evaluated for immunohistochemical, histopathologic assessments and also for tissue cytokines, oxidant and antioxidant levels.RESULTS:
Dexmedetomidine significantly ameliorated histopathologic changes such as periacinar fibrosis, acinar atrophy, lymphocytic infiltration, ductal proliferation, lipofuscin-like accumulation, and nucleus changes caused by RAI in all lacrimal gland forms (p < 0.05 for all of the parameters). However, periductal fibrosis was improved significantly only in EG (p = 0.049), and mast cell infiltration was improved significantly only in IG (p = 0.038) in Dexmedetomidine groups. There was a significant decrease in the elevated caspase-3 and TUNEL levels after RAI administration in the Dexmedetomidine group in all lacrimal gland forms (p < 0.05 for all parameters). Dexmedetomidine attenuated NF-kb, TNF-α, and IL-6 levels significantly diminished total oxidant status and raised total antioxidant status levels (p < 0.05 for all parameters).CONCLUSIONS:
The results of this study demonstrated that following RAI, Dexmedetomidine diminished inflammation, tissue cytokine levels, and apoptosis and ameliorated impaired histopathologic patterns of the lacrimal glands.Palavras-chave
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Dexmedetomidina
/
Aparelho Lacrimal
Limite:
Animals
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article