Xin-Sheng Zhang1, Bi-De Zhu, Xiao-Qin Hung, Yong-Feng Chen. 1. Department of Histology, Embryology and Neurobiology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu 610041, China.
Abstract
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. CONCLUSION: 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.
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 anemiamice, 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 anemiamice 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. CONCLUSION: 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.