Rapid inhibitory effect of glucocorticoids on peak of Ca2+i and PLC in airway smooth muscle.
- Author:
Hai-Wen SUN
1
;
Lei LIU
;
Ming-Gao LI
;
Chun-Lei JIANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Calcium; metabolism; Cells, Cultured; Dexamethasone; pharmacology; Glucocorticoids; pharmacology; Guinea Pigs; Male; Mifepristone; pharmacology; Muscle, Smooth; drug effects; metabolism; Phospholipase C beta; metabolism; Rats; Rats, Sprague-Dawley; Trachea; cytology
- From: Chinese Journal of Applied Physiology 2010;26(4):440-443
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEIn this study, we pretreated the mice ASMCs by dexamethasone (Dex) within 10 min, to test the peak of [Ca2+]i and phospho-PLCbeta (ser1105) in the cells by treated with Ach.
METHODSThe peak of [Ca2+]i was measured by Fura-2/AM methods and the phospho-PLCbeta-ser1105 was by Western blot, and compared with dexamethasone pretreated groups. Glucocorticoid receptor antagonist RU486 and the protein synthesis inhibitor cycloheximide groups were settled in our study.
RESULTSGlucocorticoids (GCs) significantly decreased the resting values and peak of [Ca2+]i elevation and elevated the intracellular levels of phospho-PLCbeta (ser1105) in 10 min. Neither the RU486 nor cycloheximide could alter the inhibitory effects of glucocorticoids stated above.
CONCLUSIONOur results demonstrate that glucocorticoids exert rapid inhibitory effects. The series of signal changes in this process that restrain the peak of [Ca2+]i may be responsible for the rapid nongenomic inhibitory effects of GCs by reducing the activity of PLC.
