인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
DBpia AI
AI 에이전트
AI 아이디어
AI 리더
AI 뷰어
Citeasy
크롬 서지관리 다운로드
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
Abstract Objectives Valosin-containing protein (p97/VCP) and its cofactor, small p97/VCP-interacting protein (SVIP), are involved in the endoplasmic reticulum - associated degradation pathway (ERAD). We investigated the cellular localization of vitamin D receptor (VDR), ERAD, and autophagic proteins (LC3B and p62) in rat brain tissue. Methods There were four groups consisting of 24 Wistar albino rats: control and treatment groups for vitamin D, omega-3, and both vitamin D and omega-3. Brain tissues were stained with hematoxylin-eosin, azan trichrome, and toluidine blue for histopathological evaluation. The immunohistochemistry assay was performed for VDR, p97/VCP, SVIP, LC3B, and p62 in rat brain sections. Results The immunoexpression of VDR and p97/VCP was significantly increased in hippocampus and cortex of brain tissue from the vitamin D-supplemented group. Furthermore, the protein expression level of SVIP reached the highest level in vitamin D-treated group. LC3B and p62 revealed reduced expressions in vitamin D-treated group in rat brain and hippocampus, in contrast to p97/VCP, SVIP, and VDR. Conclusions Vitamin D and omega-3 supplementations had no negative effects at a cellular level on hippocampus and cortex of the brain tissue. Vitamin D increased the expression of the proteins that are related to the ERAD pathway, whereas it reduced the expression of the proteins in the autophagy pathway. Also, in this study, SVIP expressions were shown in rat hippocampus and cortex of the brain tissue.
#Endoplasmic reticulum
#Autophagy
#Cell biology
#Protein expression
#Endoplasmic-reticulum-associated protein degradation
#Protein degradation
#Degradation (telecommunications)
#Omega
#Chemistry
#Vitamin D and neurology
#Biochemistry
#Biology
#Unfolded protein response
#Endocrinology
#Apoptosis
#Computer science
#Gene
#Philosophy
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