Tauroursodeoxycholic acid suppresses endoplasmic reticulum stress in pulmonary tissues of intermittent hypoxia mice.
10.11817/j.issn.1672-7347.2015.11.001
- Author:
Zhihui SHI
1
;
Linhao XU
1
;
Rui ZHOU
1
Author Information
1. Department of Respiration, Second Xiangya Hospital, Central South University, Changsha 410011, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
drug effects;
Caspase 12;
metabolism;
Caspase 3;
metabolism;
Disease Models, Animal;
Endoplasmic Reticulum Stress;
drug effects;
Heat-Shock Proteins;
metabolism;
Hypoxia;
physiopathology;
Lung;
drug effects;
Mice;
Mice, Inbred C57BL;
Real-Time Polymerase Chain Reaction;
Taurochenodeoxycholic Acid;
pharmacology;
Transcription Factor CHOP;
metabolism
- From:
Journal of Central South University(Medical Sciences)
2015;40(11):1165-1172
- CountryChina
- Language:Chinese
-
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.
