补血I号对环磷酰胺致血小板减少小鼠模型病理机制研究

Study on Pathological Mechanism of Using No.1 Buxue Decoction for Thrombocytopenia Induced by CTX in Mice Model

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（P0.01～0.001）;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（P0.05）;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（P0.01）,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（P0.001）。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： Observing No. 1 Buxue Decoction of CTX pathomechanism in mice model, discussing the possible mechanism of action. Methods： Intraperitoneal injection of giving CTX for building, executing each group of mice after 1 hour, immediately taking entire section femoral organization into fixed in FAA solution, HE staining and observed under light microscopy bone marrow nucleated cells number and the number of megakaryocyte, immunohistochemical detection of caspase 3 and Ki- 57 protein content. Results ： No. 1 Buxue Decoction of high, middle dose group and positive group mice hone marrow nucleated cell area, integral optical density than the model group increased significantly, the difference was statistically significant （P 〈 0. 01 and 0. 001 ） ; No. 1 Buxue Decoction in high dose group and positive group mice bone marrow megakaryocyte number were more than the model group, the difference was statistically significant （ P 〈0.05 ） ; No. 1 Buxue Decoction of high, middle 〈lose group and positive group mice bone marrow nucleated cells Ki-67 integral optical density were more than the model group, the difference was statistically significant （ P 〈0. 01 ）, No.1 Buxue Decoction of high, medium and low dose group and positive group mice bone marrow nucleated cells caspase3 integral optical density were more than the model group, the difference was statistically significant （P 〈0. 001 ）. Conclusion： The No. 1 Buxue Decoction can be raised by CTX induced thrombocytopenia in mice mcdel bone marrow cell proliferation, to reduce the apoptosis of bone marrow ceils, thus improve the bone marrow hematopoietic cells, play on the therapeutic effect of CTX pathomechanism mice model.