Effect of Norcantharidin on Hematopoietic Function in Leucopenia Model Rat Induced by Cyclophosphamide.
- Author:
Dan ZHENG
1
;
Qi-Ming SHA
2
;
Jian-Qing WANG
3
;
Zheng-Mei LIU
1
;
Xiu-Fang WAN
1
;
Guo-Chuan WANG
1
;
Ya-Li ZHANG
4
;
Guo-Zhen YANG
5
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Bone Marrow; Bone Marrow Cells; Bridged Bicyclo Compounds, Heterocyclic; Cell Cycle; Cell Proliferation; Cyclophosphamide; Disease Models, Animal; Flow Cytometry; Hematologic Diseases; Hematopoiesis; Rats; Rats, Sprague-Dawley
- From: Journal of Experimental Hematology 2015;23(3):826-831
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effect and mechanism of norcantharidin (NCTD) on hematopoiesis function in leucopenia model rat induced by cyclophosphamide (CTX).
METHODSLeucopenia model was replicated in SD rat with cyclophosphamide(CTX) and model animal was treated with NCTD. Peripheral blood and bone marrow tissue samples were collected from the rats in each experimental group. Peripheral white blood cells (WBC) were counted and analyzed by automatic blood cell analyzer. Histopathologic changes of the biopsied bone marrow tissues were observed by histopathological techniques. The cell cycle and apoptosis rate of bone marrow cells were detected by flow cytometry. Immunohistochemical method was applied to observe the expression of apoptosis-related proteins BCL-2 and BAX in bone marrow.
RESULTSAfter NCTD treatment in model rats, the WBC count of peripheral blood obviously increased, the cell structure of bone tissue significantly recovered, NCTD could promote the cell proliferation and cycle changes of bone marrow cells, inhibit the bone marrow cell apoptosis and necrosis induced with CTX, up-regulate the expression of apoptosis-related protein BCL-2 and downregulated the BAX.
CONCLUSIONNCTD can stimulate the bone marrow hematopoiesis and promote recovery of peripheral white blood cell level in the leukopenia model induced by CTX, and its mechanism may be related with NCTD regulating bone marrow cell cycle and with NCTD inhibiting cell apoptosis.