Protective effect of carbenoxolone on ER stress-induced cell death in hypothalamic neurons.
Biochem Biophys Res Commun
; 468(4): 793-9, 2015 Dec 25.
Article
en En
| MEDLINE
| ID: mdl-26577412
ABSTRACT
Hypothalamic endoplasmic reticulum (ER) stress is known to be increased in obesity. Induction of ER stress on hypothalamic neurons has been reported to cause hypothalamic neuronal apoptosis and malfunction of energy balance, leading to obesity. Carbenoxolone is an 11ß-hydroxysteroid dehydrogenase type 1 (11ß-HSD1) inhibitor that converts inactive glucocorticoid into an active form. In addition to its metabolic effect via enzyme inhibitory action, carbenoxolone has shown anti-apoptotic activity in several studies. In this study, the direct effects of carbenoxolone on ER stress and cell death in hypothalamic neurons were investigated. Carbenoxolone attenuated tunicamycin induced ER stress-mediated molecules such as spliced XBP1, ATF4, ATF6, CHOP, and ROS generation. In vivo study also revealed that carbenoxolone decreased tunicamycin-induced ER stress in the hypothalamus. In conclusion, the results of this study show that carbenoxolone has protective effects against tunicamycin induced-ER stress and apoptosis in hypothalamic neurons, suggesting its direct protective effects against obesity. Further study is warranted to clarify the effects of carbenoxolone on hypothalamic regulation of energy balance in obesity.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Estrés Fisiológico
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Carbenoxolona
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Apoptosis
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Retículo Endoplásmico
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Hipotálamo
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Neuronas
Límite:
Animals
Idioma:
En
Revista:
Biochem Biophys Res Commun
Año:
2015
Tipo del documento:
Article
País de afiliación:
Corea del Sur