An experimental study on the role of PGE2 and cAMP on the postburn change of the granulopoiesis in bone marrow in burned mice with endotoxemia.
- Author:
De-Bing XIANG
1
;
You-Sheng LIU
;
Shui-Ming WANG
;
Xiao-Dong WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Bone Marrow Cells; pathology; Burns; complications; metabolism; Cyclic AMP; metabolism; Cyclooxygenase 2; metabolism; Dinoprostone; metabolism; Endotoxemia; etiology; metabolism; Granulocytes; pathology; Male; Mice; Mice, Inbred Strains
- From: Chinese Journal of Burns 2003;19(2):78-81
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of PGE(2) and cAMP in the postburn change in granulopoiesis in bone marrow in burned mice with endotoxemia.
METHODSOne hundred and seventy eight mice were randomly divided into burn with LPS administration, simple burn, simple LPS administration and control (injection of normal saline) groups. The COX-2 expression and the contents of PGE(2) and cAMP in myeloid cells in injured mice in all groups were determined by RIA (radioimmuno-assay) within 1 postburn week and immunohistochemistry methods. At the same time the change in granulopoiesis was dynamically observed.
RESULTSThe granulopoiesis was enhanced slightly at the early stage of burn and with endotoxin challenge, followed by suppression. The COX-2 expression in myeloid cells the contents of PGE(2) on supernatant of marrow cells and intracellular cAMP in the myeloid cells was increased at 12 postburn hour (PBH) up to 5 postburn day (PBD). Furthermore, the change in the cAMP was evidently and positively correlated with that of PGE(2) (r = 0.978, P < 0.01), but was negatively correlated with that of CFU-GM (r = -0.971, P < 0.01)
CONCLUSIONPGE(2) might play pivotal roles in the postburn granulopoiesis suppression in bone marrow during endotoxemia. This effect might be accomplished by its ligating to its special receptor and to activate adenylate cyclase so as to increase the intracellular content of cAMP in bone marrows.