Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage

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dc.authoridYavuz, Hayrettin/0000-0001-5190-7022
dc.contributor.authorDuman, Gulhan
dc.contributor.authorAlcigir, Mehmet Eray
dc.contributor.authorYavuz, Hayrettin
dc.date.accessioned2025-01-21T16:34:37Z
dc.date.available2025-01-21T16:34:37Z
dc.date.issued2021
dc.departmentKırıkkale Üniversitesi
dc.description.abstractOBJECTIVE: Congenital hypothyroidism (CH) is literally described as congenital thyroid hormone imperfection. The primary objective of this research was to reveal the possible relation between receptor-acting protein kinase 3 (RIPK3) activity and neuronal damages in rat pups with CH. In addition, we evaluated the favorable impacts of 3.6-dibromo-alpha-([phenylamino] methyl)-9H-carbazole-9-ethanol (P7C3) reducing RIPK3 activity. METHODS: Adult rats were accordingly assigned into four groups: Group 1, which is called congenital hypothyroid; Group 2, which is called congenital hypothyroid administered P7C3; Group 3, called CH administered P7C3 and L-thyroxine; and Group 4, control group. RIPK3 level in plasma concentration and its expression in tissue was determined in all groups. RESULTS: Increased RIPK3 expressions were detected as high in the CH group when it is compared to the control group. Furthermore; the expressions in neuronal cytoplasm were found similar among Groups II and III. RIPK3 expressions in those two groups were relatively higher than in the control group. Most reacted parts of the brain were especially Purkinje cells in the cerebellum. CONCLUSION: It is concluded that there is excellent parallelism among damaged neurons and high RIPK3 activity in CH pathogenesis. P7C3 compounds may have a safeguarding impact on CH due to decreasing RIPK3 activity.
dc.identifier.doi10.14744/nci.2021.26043
dc.identifier.endpage478
dc.identifier.issn2148-4902
dc.identifier.issue5
dc.identifier.pmid34909585
dc.identifier.startpage472
dc.identifier.trdizinid508447
dc.identifier.urihttps://doi.org/10.14744/nci.2021.26043
dc.identifier.urihttps://search.trdizin.gov.tr/tr/yayin/detay508447
dc.identifier.urihttps://hdl.handle.net/20.500.12587/23993
dc.identifier.volume8
dc.identifier.wosWOS:000714065600006
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakTR-Dizin
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherKare Publ
dc.relation.ispartofNorthern Clinics of Istanbul
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_20241229
dc.subjectCongenital hypothyroidism; rat; receptor-acting protein kinase 3 activity; 3.6-Dibromo-alpha-([phenylamino] methyl)-9H-carbazole-9-ethanol
dc.titleNecroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage
dc.typeArticle

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