[Effect of salidroside on bone marrow cell cycle and expression of apoptosis-related proteins in bone marrow cells of bone marrow depressed anemia mice].
OBJECTIVE
To examine the effect of salidroside on bone marrow cell cycle and expression of apoptosis-related proteins in bone marrow cells (BMCs) of bone marrow depressed anemia mice, and to explore its mechanism for hematopoietic regulation.


METHODS
The effect of salidroside on peripheral blood cells, BMCs, and bone marrow cell cycle in bone marrow depressed anemia mice was detected by automatic blood cell analysator, white blood count and flow cytometry (FCM)respectively,and the expression of Bcl-2 and Bax of BMCs was detected by immunohistochemistry method simultaneously.


RESULTS
It was found that low-dose and high-dose salidroside obviously elevated white blood cells and BMCs, that low-dose salidroside significantly increased platelets and promoted G0/G1-S phase and S-G2/M phase transition of BMCs, that high-dose salidroside markedly promoted S-G2/M phase transition of BMCs, and that both low-dose and high-dose salidroside obviously elevated the proliferation index and the ratio of G2/M phase cells. Additionally, the expression of Bcl-2 in BMCs was increased in low-dose and high-dose salidroside groups, especially the increase was significant in the low-dose salidroside group; moreover, the expression of Bax in BMCs was reduced significantly in both low-dose and high-dose salidroside groups.


CONCLUSIONS
These data suggest that salidroside may promote the recovery of hematopoietic function of the bone marrow depressed anemia in mice by ending off G0/G1-phase arrest, accelerating G0/G1-S phase and S-G2/M phase transition, up-regulating Bcl-2 expression, down-regulating Bax expression, and inhibiting BMCs apoptosis.
Zhang
Xin-Sheng
XS
Department of Histology, Embryology and Neurobiology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu 610041, China.
Zhu
Bi-De
BD
Hung
Xiao-Qin
XQ
Chen
Yong-Feng
YF
D000741:Anemia, Aplastic / Q000097:blood / Q000503:physiopathology; D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D001854:Bone Marrow Cells / Q000378:metabolism / Q000473:pathology*; D002453:Cell Cycle / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D005960:Glucosides / Q000494:pharmacology*; D006410:Hematopoiesis / Q000187:drug effects*; D006412:Hematopoietic Stem Cells / Q000166:cytology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010636:Phenols / Q000494:pharmacology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis* / Q000235:genetics; D011897:Random Allocation; D029771:Rhodiola / Q000737:chemistry; D051028:bcl-2-Associated X Protein / Q000096:biosynthesis / Q000235:genetics
C494827:Bax protein, mouse; D005960:Glucosides; D010636:Phenols; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; C009172:rhodioloside