Tauroursodeoxycholic acid suppresses endoplasmic reticulum stress in pulmonary tissues of intermittent hypoxia mice / 中南大学学报(医学版)
Journal of Central South University(Medical Sciences)
;
(12): 1165-1172, 2015.
Artigo
em Chinês
| WPRIM
| ID: wpr-815359
ABSTRACT
OBJECTIVE@#To explore the mechanism of tauroursodeoxycholic acid (TUDCA) in suppressing apoptosis in pulmonary tissues of intermittent hypoxia (IH) mice model.
@*METHODS@#A total of 32 C57 mice were randomly divided into a control group, a TUDCA group, an IH group and an IH+TUDCA group (8 mice per group). The mice were put in specially designed chambers and exposed to IH treatment for 4 weeks. In the chambers, oxygen levels repeatedly decreased from 21% to 10% and recovered from 10% to 21%, lasting for 8 hours in every day. After 4 weeks of IH exposure, the expression levels of caspase-12 and cleaved caspase-3 in pulmonary tissues were detected by Western blot. Meanwhile, the expression levels of glucose regulated protein-78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP) were quantified by Western blot, immunochemistry and real-time PCR.
@*RESULTS@#Compared with the control group, the expression levels of caspase-12, cleaved caspase-3, GRP78 and CHOP were increased in the IH group (all P<0.01). TUDCA treatment could reduce these proteins expression (all P<0.05).
@*CONCLUSION@#Endoplasmic reticulum stress-mediated apoptosis can be activated in pulmonary tissues after chronic IH exposure, and TUDCA can reduce the cellular apoptosis via suppressing endoplasmic reticulum stress.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
Ácido Tauroquenodesoxicólico
/
Apoptose
/
Modelos Animais de Doenças
/
Fator de Transcrição CHOP
/
Caspase 3
/
Caspase 12
/
Reação em Cadeia da Polimerase em Tempo Real
/
Estresse do Retículo Endoplasmático
/
Proteínas de Choque Térmico
Tipo de estudo:
Estudo prognóstico
Limite:
Animais
Idioma:
Chinês
Revista:
Journal of Central South University(Medical Sciences)
Ano de publicação:
2015
Tipo de documento:
Artigo
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