OGP_(10～14)及其衍生物改善化疗后小鼠造血功能的研究

The Effects of OGP_(10～14) and its Derivatives on Hematopoiesis in Mice Treated By Cyclophosphamide

目的观察人工合成的成骨生长肽羧基端片段(OGP(10～14))及其衍生物G38I、G38K对环磷酰胺化疗后骨髓抑制小鼠外周血象和骨髓造血功能的影响。方法 40只BALB/C小鼠随机分为5组,均给予环磷酰胺(CTX)腹腔注射诱导骨髓抑制。分别给予OGP(10～14)、G38I、G38K或粒细胞集落刺激因子(G-CSF)治疗,未给予治疗的CTX组为阴性对照。实验中多次采集小鼠外周血测定外周血象并于注射CTX后第7天处死。观察骨髓有核细胞数的变化。结果 CTX组小鼠注射CTX后外周血白细胞和血小板下降,出现骨髓造血抑制。注射CTX前OGP(10～14)及其衍生物对小鼠外周血象无明显影响。注射CTX后OGP(10～14)组和G38I组外周血白细胞较CTX组显著升高,疗效与G-CSF接近,G38I组和G38K组血小板升高。OGP(10～14)及其衍生物G38I、G38K和G-CSF处理使小鼠骨髓有核细胞数增多,OGP(10～14)和G38I疗效更优于G38K。结论 OGP(10～14)及其衍生物G38I、G38K促进骨髓抑制小鼠外周血白细胞和血小板升高,刺激骨髓造血干细胞活性,加速骨髓造血功能的恢复。

Objective To investigate the effects of OGP（10-14） and its derivatives G38I, G38K on peripheral blood and bone marrow hematopoiesis in mice av.ated by cyclophosphamide（CTX）. Methods Forty BALB/C mice were randomly divided into 5 groups. The marrow ablation was carded out by intraperitoneal injection of CTX. The mice were treated by OGP（10-14）, G38I, G38K or granulocyte-colony stimulating factor（G-CSF） respectively while the CTX group was negative control. The peripheral blood were collected and cells counts were performed four times on the same animal before and after CTX injection. All mice were sacrificed on the 7th day after CTX injection. Bone marrow nucleated cells（BMNC） were studied. Results The white blood cells（WBC） and platelets（PLT）counts decreased after CTX injection in CTX group. OGP（10-14） and its derivatives hadn＇t significant effects on peripheral blood before CTX injection but the WBC counts of OGP（10-14） and G38I were increased compared with that in CTX group and similar with G-CSF treated group after CTX injection. PLT were increased in G38I and G38K groups. The BMNC were increased in OGP（10-14）, G38I, G38K and G-CSF group. Between the treated groups, OGP（10-14） and G38I were more efficient compared to G38K. Conclusion OGP（10-14） and its derivatives G38I, G38K may enhance the WBC and PLT of peripheral blood in mice with bone marrow injury, mobilized the hematopoific stem cells and accelerate recovery of hematopoiesis of bone marrow.