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[川芎嗪对免疫性再生障碍性贫血小鼠骨髓微环境改善作用的研究]

[Study on the improvement of bone marrow microenvironment by ligustrazine in immune-induced aplastic anemia mice].

作者信息

Sun H, Shu Y, Liu W

机构信息

Department of Internal Medicine, Tongji Hospital, Tongji Medical University, Wuhan 430030.

出版信息

Zhonghua Xue Ye Xue Za Zhi. 1998 Apr;19(4):178-80.

Abstract

OBJECTIVE

To explore the effects of ligustrazine on bone marrow microenvironment and its mechanism in aplastic anemia (AA).

METHODS

Each immune-induced AA mouse was gastric fed by 4 mg ligustrazine twice a day. On the 10th day, the ulnar bone marrow partial pressure of oxygen (PbO2) was determined in vivo by a PO2 sensory needle. Then the histological features, fibroblastic colony forming unit (CFU-F) yields and the adhesive function of stromal cells of the bone marrow were assayed in vitro.

RESULTS

The PbO2 in ligustrazine-treated group was 10.32 +/- 1.27 kPa, while in AA group was 4.32 +/- 2.86 kPa (P < 0.001). In AA group, the microvessels were expanded, broken and being stasis. The percentage of hematopoietic tissue volume was 24.9% +/- 9.6% and the CFU-F yields was 12.5 +/- 7.3/2 x 10(6) BMNC. The microvessels in ligustrazine group were more clear and intact, not being broken and had no stasis. The percentage of hematopoietic tissue volume was 52.8% +/- 15.6% and the CFU-F yields was 31.5 +/- 10.6/2 x 10(6) BMNC. In ligustrazine group, the adhesive function of stromal cell layer cultured with bone marrow nucleated cells from normal mice was 72.7% +/- 7.8%, which was not different from that in normal group (73.4% +/- 3.4%), but much higher than that in AA group (56.2% +/- 9.8%, P < 0.01).

CONCLUSION

Ligustrazine can promote the rehabilitation of bone marrow microvessels in AA mice, increasing the oxygen supply for bone marrow microenvironment, promoting the growth of stromal cells and strengthening their adhesive function. Ligustrazine enbances the bone marrow hematopoietic cells proliferation by improving their microenvironment.

摘要

目的

探讨川芎嗪对再生障碍性贫血(AA)小鼠骨髓微环境的影响及其作用机制。

方法

对每只免疫诱导的AA小鼠每天经胃给予4mg川芎嗪,分两次给药。第10天,用PO2传感针在体内测定尺骨骨髓氧分压(PbO2)。然后在体外检测骨髓的组织学特征、成纤维细胞集落形成单位(CFU-F)产量及基质细胞的黏附功能。

结果

川芎嗪治疗组的PbO2为10.32±1.27kPa,而AA组为4.32±2.86kPa(P<0.001)。AA组微血管扩张、破裂并伴有淤血。造血组织体积百分比为24.9%±9.6%,CFU-F产量为12.5±7.3/2×10(6)骨髓单个核细胞(BMNC)。川芎嗪组微血管更清晰、完整,无破裂和淤血。造血组织体积百分比为52.8%±15.6%,CFU-F产量为31.5±10.6/2×10(6)BMNC。川芎嗪组用正常小鼠骨髓有核细胞培养的基质细胞层黏附功能为72.7%±7.8%,与正常组(73.4%±3.4%)无差异,但远高于AA组(56.2%±9.8%,P<0.01)。

结论

川芎嗪可促进AA小鼠骨髓微血管的修复,增加骨髓微环境的氧供应,促进基质细胞生长并增强其黏附功能。川芎嗪通过改善骨髓微环境增强骨髓造血细胞增殖。

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