红景天苷对骨髓抑制贫血小鼠骨髓细胞周期和凋亡相关蛋白表达的影响

目的 观察红景天苷对骨髓抑制贫血小鼠骨髓细胞周期和凋亡相关蛋白表达的影响，并探讨其造血调控作用机制。方法 用全自动血细胞分析仪、白细胞计数法和流式细胞术（FCM）分别检测红景天苷对骨髓抑制贫血小鼠外周血、骨髓有核细胞以及骨髓细胞周期的影响，同时用免疫组织化学方法检测各组骨髓细胞凋亡相关蛋白Bcl-2和Bax的表达情况。结果 低剂量和高剂量红景天苷能明显升高外周血白细胞（WBC）和骨髓有核细胞（BMC）数，低剂量红景天苷能明显升高外周血血小板（PLT）数，促进骨髓G0／G1期细胞向S期细胞以及S期细胞向G2／M期细胞的转化，而高剂量红景天苷具有明显促进S期细胞向G2／M期细胞转化的能力，从而导致高、低剂量组G2／M期细胞比例明显升高，增殖指数（PI）也明显升高。另外，高、低剂量红景天苷都能促进骨髓细胞中Bcl-2的表达。其中低剂量红景天苷的促进作用更为明显。同时，高、低剂量红景天苷也都能明显降低骨髓细胞中Bax的表达。结论 红景天苷可能通过促使骨髓抑制贫血小鼠骨髓细胞解除G0／G1期阻滞，加速骨髓G0／G1期细胞向S期细胞、S期细胞向G2／M期细胞的转化以及升高骨髓细胞Bcl-2的表达、降低Bax的表达来抑制骨髓细胞凋亡，促进骨髓造血功能的恢复。

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 G_0/G_1-S phase and S-G_2/M phase transition of BMCs,that high-dose salidroside markedly promoted S-G_2/M phase transition of BMCs,and that both low-dose and high-dose salidroside obviously elevated the proliferation index and the ratio of G_2/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 G_0/G_1-phase arrest,accelerating G_0/G_1-S phase and S-G_2/M phase transition,up-regulating Bcl-2 expression,down-regulating Bax expression,and inhibiting BMCs apoptosis.