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目的:观察补血I号对环磷酰胺致血小板减少小鼠模型治疗作用,探讨其可能的病理机制。方法:腹腔注射给予环磷酰胺进行造模,给药1小时后处死每组小鼠,立即取全段股骨组织投入FAA溶液中固定,HE染色,在光镜下观察骨髓有核细胞数目及巨核细胞数量,免疫组化检测caspase-3和Ki-57蛋白含量。结果:补血Ⅰ号高、中剂量组和阳性组小鼠骨髓有核细胞面积、积分光密度比模型组显著增多,差异有统计学意义(P<0.01~0.001);补血Ⅰ号高剂量组和阳性组小鼠骨髓巨核细胞数目比模型组显著增多,差异有统计学意义(P<0.05);补血Ⅰ号高、中剂量组和阳性组小鼠骨髓有核细胞Ki-67积分光密度比模型组显著增多,差异有统计学意义(P<0.01),补血Ⅰ号高、中、低剂量组和阳性组小鼠骨髓有核细胞Caspase3积分光密度比模型组显著增多,差异有统计学意义(P<0.001)。结论:补血Ⅰ号可通过提高环磷酰胺致血小板减少小鼠模型骨髓细胞增殖、降低骨髓细胞凋亡,从而提高骨髓造血细胞数量,发挥对环磷酰胺致血小板减少小鼠模型的治疗作用。
Objective: To observe the effect of Buixue I on cyclophosphamide-induced thrombocytopenic mouse model and explore its possible pathological mechanism. METHODS: Cyclophosphamide was given intraperitoneally to make model. One hour later, mice in each group were sacrificed. The whole femur tissue was fixed in FAA solution and stained with hematoxylin-eosin (HE). The numbers of nucleated cells and megakaryocytes Cell number, immunohistochemistry detection of caspase-3 and Ki-57 protein content. Results: Compared with the model group, the area of nucleated cells and the integral optical density of the mice in the high, medium and high doses of Buxue Ⅰ group were significantly increased (P <0.01 ~ 0.001) Compared with the model group, the number of bone marrow megakaryocytes in the positive group was significantly increased (P <0.05). Ki-67 integral optical density ratio (P <0.01). The optical density of Caspase3 of bone marrow nucleated cells in the high, middle and low doses of Xuebian Ⅰ group and the positive group were significantly increased compared with the model group, the difference was statistically significant (P < P <0.001). Conclusion: Buxue Ⅰ can increase the number of bone marrow hematopoietic cells and increase the therapeutic effect of cyclophosphamide-induced thrombocytopenic mouse model by increasing the proliferation of bone marrow cells induced by cyclophosphamide-induced thrombocytopenia in mice and decreasing the apoptosis of bone marrow cells.