目的了解血小板第４因子（ＰＦ４）和四肽Ｎ乙酰丝天赖脯（ＡｃＳＤＫＰ）对５氟尿嘧啶（５ＦＵ）处理后小鼠体内造血的作用。方法实验鼠用ＰＦ４（４０μｇ／ｋｇ）或ＡｃＳＤＫＰ（４μｇ／ｋｇ）注射２次，间隔６小时，第２次注射后２０小时再注射５ＦＵ（１５０ｍｇ／ｋｇ）。第６，８和１３天时，检查高增殖潜能的集落形成细胞（ＨＰＰＣＦＣ）、红系爆式集落形成单位（ＢＦＵＥ）、粒巨噬系集落形成单位（ＣＦＵＧＭ）、巨核系集落形成单位（ＣＦＵＭＫ）及巨核细胞（ＭＫ）。结果ＰＦ４或ＡｃＳＤＫＰ可促使６～８天的ＨＰＰＣＦＣ以及８天的ＢＦＵＥ和ＣＦＵＧＭ明显增加；ＰＦ４还能促进８天的ＣＦＵＭＫ和ＭＫ增加，但ＡｃＳＤＫＰ则无此作用。结论ＰＦ４和ＡｃＳＤＫＰ虽然对巨核祖细胞的作用不同，但它们均能加速体内ＨＰＰＣＦＣ、ＣＦＵＧＭ和ＢＦＵＥ的恢复，这两种分子有可能具有保护造血细胞抵抗化疗药物杀伤的作用。 Objective To investigate the effect of platelet factor 4 (PF4) and tetrapeptide AcSDKP on hematopoiesis in 5-fluorouracil (5FU) -treated mice. Methods Experimental mice were injected twice with PF4 (40μg / kg) or AcSDKP (4μg / kg) at an interval of 6 hours and injected with 5FU (150mg / kg) 20 hours after the second injection. On the 6th, 8th and 13th days, the colony forming cells (HPPFCF), erythrocytic burst forming units (BFUE), granulocyte  macrophage colony forming unit (CFUGM) Department of colony-forming units (CFU MK) and megakaryocytes (MK). Results PF4 or AcSDKP can promote 6 to 8 days of HPP FCF and 8 days of BFU E and CFU GM significantly increased; PF4 can also promote 8 days CFU MK and MK increased, but AcSDKP no such effect. Conclusion Although PF4 and AcSDKP have different effects on megakaryocyte progenitor cells, they both accelerate the recovery of HPPCFC, CFUGM and BFUE in vivo. These two molecules may have the effect of protecting hematopoietic cells against chemotherapeutic drug killing.