Role of autophagy in lysophosphatidylcholine-induced apoptosis in mouse Leydig cells.
Leydig cells
apoptosis
autophagy
lysophosphatidylcholine
oxidative stress
Journal
Environmental toxicology
ISSN: 1522-7278
Titre abrégé: Environ Toxicol
Pays: United States
ID NLM: 100885357
Informations de publication
Date de publication:
Nov 2022
Nov 2022
Historique:
revised:
10
07
2022
received:
10
02
2022
accepted:
21
07
2022
entrez:
10
10
2022
pubmed:
11
10
2022
medline:
12
10
2022
Statut:
ppublish
Résumé
Lysophosphatidylcholine (LPC), a major class of glycerophospholipids ubiquitously present in most tissues, plays a dominant role in many diseases, while it is still unknown about the potential mechanism of LPC affecting the testicular Leydig cells. In the present study, mouse TM3 Leydig cells in vitro were treated with LPC for 48 h. LPC was found to significantly induce apoptosis and oxidative stress of mouse TM3 Leydig cells; while inhibition of oxidative stress by N-acetyl-L-cysteine, an inhibitor of oxidative stress, could rescue the induction of apoptosis, indicating that LPC induced apoptosis of mouse TM3 Leydig cells via oxidative stress. Interestingly, LPC was showed to inhibit autophagy; however, induction of autophagy by rapamycin significantly alleviated the induction of apoptosis by LPC. Taken together, oxidative stress was involved in LPC-induced apoptosis of mouse TM3 Leydig cells, and autophagy might play a protective role in LPC-induced apoptosis.
Substances chimiques
Glycerophospholipids
0
Lysophosphatidylcholines
0
Sirolimus
W36ZG6FT64
Acetylcysteine
WYQ7N0BPYC
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2756-2763Subventions
Organisme : Educational Committee of Jiangxi Province
ID : GJJ190931
Organisme : Natural Science Foundation of Jiangxi Province
ID : 20212ACB206036
Organisme : Major Discipline Academic and Technical Leaders Training Program of Jiangxi Province
ID : 20204BCJ22031
Organisme : National Natural Science Foundation of China
ID : 82060278
Organisme : National Natural Science Foundation of China
ID : 81660255
Informations de copyright
© 2022 Wiley Periodicals LLC.
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