title: Morphologic Damage of Rat Alveolar Epithelial Type II Cells Induced by Bile Acids Could Be Ameliorated by Farnesoid X Receptor Inhibitor Z-Guggulsterone In Vitro.
abstract: Objective. To determine whether bile acids (BAs) affect respiratory functions through the farnesoid X receptor (FXR) expressed in the lungs and to explore the possible mechanisms of BAs-induced respiratory disorder. Methods. Primary cultured alveolar epithelial type II cells (AECIIs) of rat were treated with different concentrations of chenodeoxycholic acid (CDCA) in the presence or absence of FXR inhibitor Z-guggulsterone (GS). Then, expression of FXR in nuclei of AECIIs was assessed by immunofluorescence microscopy. And ultrastructural changes of the cells were observed under transmission electron microscope and analyzed by Image-Pro Plus software. Results. Morphologic damage of AECIIs was exhibited in high BAs group in vitro, with high-level expression of FXR, while FXR inhibitor GS could attenuate the cytotoxicity of BAs to AECIIs. Conclusions. FXR expression was related to the morphologic damage of AECIIs induced by BAs, thus influencing respiratory functions.
authors.affiliation: Department of Physiology, Southern Medical University, 1838 Guangzhou Avenue, North Baiyun District, Guangzhou, Guangdong 510080, China.
authors.forename: Jieqin
authors.identifier: 0000-0002-3343-5639
authors.initials: J
authors.lastname: Wang
authors.affiliation: Institute of Genetic Engineering, Southern Medical University, 1838 Guangzhou Avenue, North Baiyun District, Guangzhou, Guangdong 510080, China.
authors.forename: Yaowei
authors.initials: Y
authors.lastname: Huang
authors.affiliation: Department of Physiology, Southern Medical University, 1838 Guangzhou Avenue, North Baiyun District, Guangzhou, Guangdong 510080, China.
authors.forename: Xusheng
authors.initials: X
authors.lastname: Hou
authors.affiliation: Department of Physiology, Southern Medical University, 1838 Guangzhou Avenue, North Baiyun District, Guangzhou, Guangdong 510080, China.
authors.forename: Wenyu
authors.initials: W
authors.lastname: Wu
authors.affiliation: Department of Physiology, Southern Medical University, 1838 Guangzhou Avenue, North Baiyun District, Guangzhou, Guangdong 510080, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Nie
authors.affiliation: Department of Physiology, Southern Medical University, 1838 Guangzhou Avenue, North Baiyun District, Guangzhou, Guangdong 510080, China.
authors.forename: Yinghong
authors.initials: Y
authors.lastname: Tian
authors.affiliation: Laboratory of Electron Microscopy, Southern Medical University, 1838 Guangzhou Avenue, North Baiyun District, Guangzhou, Guangdong 510080, China.
authors.forename: Yanmeng
authors.initials: Y
authors.lastname: Lu
authors.affiliation: Department of Physiology, Southern Medical University, 1838 Guangzhou Avenue, North Baiyun District, Guangzhou, Guangdong 510080, China.
authors.forename: Yanru
authors.identifier: 0000-0003-3812-3965
authors.initials: Y
authors.lastname: Yin
mesh_terms: D056809:Alveolar Epithelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D000818:Animals; D048430:Cell Shape / Q000187:drug effects*; D002478:Cells, Cultured; D002635:Chenodeoxycholic Acid / Q000633:toxicity*; D003593:Cytoplasm / Q000187:drug effects / Q000378:metabolism; D005455:Fluorescent Antibody Technique; D008297:Male; D011282:Pregnenediones / Q000494:pharmacology*; D017207:Rats, Sprague-Dawley; D018160:Receptors, Cytoplasmic and Nuclear / Q000037:antagonists & inhibitors* / Q000378:metabolism; D000099150:Receptor, Farnesoid X-Activated
chemical_list: D002635:Chenodeoxycholic Acid; D011282:Pregnenediones; D018160:Receptors, Cytoplasmic and Nuclear; D000099150:Receptor, Farnesoid X-Activated; C023617:pregna-4,17-diene-3,16-dione