从p38MAPK通路探讨复方参鹿颗粒对较低危MDS骨髓患者CD34细胞凋亡的影响

张旭峰; 赵琳; 徐培

doi:10.13422/j.cnki.syfjx.2017160152

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从p38MAPK通路探讨复方参鹿颗粒对较低危MDS骨髓患者CD34细胞凋亡的影响

临床 | 更新时间：2024-01-04

- 从p38MAPK通路探讨复方参鹿颗粒对较低危MDS骨髓患者CD34细胞凋亡的影响
- Effect of Compound Shenlu Granule on Apoptosis of CD34 Cells in Lower-risk MDS Bone Marrow Based on p38MAPK Pathway
- 中国实验方剂学杂志 2017年23卷第16期页码：152-157
- 作者机构：
- 作者简介：
- 基金信息：
  
  国家自然科学基金项目（81403233）
- DOI：10.13422/j.cnki.syfjx.2017160152
  中图分类号： R259
- 纸质出版日期：2017
- 稿件说明：
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张旭峰, 赵琳, 徐培. 从p38MAPK通路探讨复方参鹿颗粒对较低危MDS骨髓患者CD34细胞凋亡的影响[J]. 中国实验方剂学杂志, 2017,23(16):152-157.

ZHANG Xu-feng, ZHAO Lin, XU Pei. Effect of Compound Shenlu Granule on Apoptosis of CD34 Cells in Lower-risk MDS Bone Marrow Based on p38MAPK Pathway[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(16): 152-157.
张旭峰, 赵琳, 徐培. 从p38MAPK通路探讨复方参鹿颗粒对较低危MDS骨髓患者CD34细胞凋亡的影响[J]. 中国实验方剂学杂志, 2017,23(16):152-157. DOI： 10.13422/j.cnki.syfjx.2017160152.

ZHANG Xu-feng, ZHAO Lin, XU Pei. Effect of Compound Shenlu Granule on Apoptosis of CD34 Cells in Lower-risk MDS Bone Marrow Based on p38MAPK Pathway[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(16): 152-157. DOI： 10.13422/j.cnki.syfjx.2017160152.

摘要

目的：从p38有丝分裂原活化蛋白激酶（MAPK）通路研究复方参鹿颗粒（FSG）对较低危骨髓增生异常综合征（lower-risk MDS）骨髓CD34+细胞凋亡的影响。方法：将60例lower-risk MDS患者随机分为FSG组和安特尔治疗组，每组30例。干预3个月。观察治疗前后两组患者血常规、骨髓CD34+细胞凋亡率、骨髓单个核细胞（BMMNC）磷酸化p38（p-p38），p38，丝裂原活化蛋白激酶激酶（MKK）3/6，磷酸化p53（p-p53），B淋巴细胞瘤-2（Bcl-2），Bcl-2家族相关基因（Bcl-xl）蛋白以及p38 mRNA表达的变化。对照组7例为年龄匹配的非MDS引起的血细胞减少患者。结果：与治疗前比较，FSG组治疗后红细胞计数、血红蛋白量、血小板明显上升（P <0.05，P <0.01）；安特尔组治疗后血红蛋白量有上升趋势，白细胞、红细胞、血小板计数差异无统计学意义。与对照组比较，治疗前FSG组lower-risk MDS骨髓CD34+细胞凋亡率，p-p38，MKK3/6，p-p53蛋白表达增加，Bcl-xl蛋白表达降低（P <0.05，P <0.01），p38，Bcl-2蛋白和p38 mRNA表达无差异；FSG治疗后，CD34+细胞凋亡率，p-p38，MKK3/6，p-p53蛋白表达均降低（P <0.05），但p-p38蛋白表达仍高于对照组（P <0.05），Bcl-xl蛋白表达增高（P <0.05）。安特尔组治疗前后CD34+细胞凋亡率，p-p38，MKK3/6，p-p53，Bcl-xl蛋白表达差异均无统计学意义。对照组，lower-risk MDS患者治疗前骨髓p-p38蛋白表达和CD34+细胞凋亡率呈正相关（P <0.01）。FSG组治疗后骨髓CD34+细胞凋亡率下降与p-p38蛋白表达水平下降呈正相关（P <0.01）。结论： FSG通过调控p38MAPK通路抑制骨髓CD34+细胞凋亡，改善骨髓无效造血。

Abstract

Objective: To explore the effects of compound Shenlu granule (FSG) on the apoptosis of CD34+ cells of lower-risk myelodysplastic syndromes (MDS) bone marrow based on p38 mitogen-activated protein kinase (MAPK) pathway. Method: The 60 patients with lower-risk MDS patients were randomly divided into FSG group and andriol treatment group

30 cases in each group. All of the patients were treated for 3 months. Changes of blood routine

rates of apoptosis of CD34+cells

p-p38

p38

mitogen activated protein kinase kinase(MKK)3/6

p-p53

Bcl-xl

B-cell lymphoma-2(Bcl-2) protein and p38 mRNA expression levels in bone marrow mononuclear cells (BMMNC) were observed before and after treatment. 7 cases from control group were age-matched patients with non-MDS cytopenia. Result: After treatment

the red blood cells count

platelet count and hemoglobin count were increased in FSG group (P <0.05

P <0.01); hemoglobin count was increased in Andriol group after treatment and there was no significant difference in the count of WBC

RBC and PLT. As compared with control group

apoptosis rate of CD34+cells and expression levels of p-p38

MKK3/6

p-p53 protein were higher

and expression of Bcl-xl was lower in FSG group (P <0.05

P <0.01); while there was no significant difference in p38

Bcl-2 protein expression and p38 mRNA expression. After FSG treatment

CD34+cell apoptosis rate and levels of p-p38

MKK3/6

p-p53 protein expression in FSG group were lower (P <0.05)

p-p38 and Bcl-xl protein expression levels were higher than those in control group (P <0.05). There was no significant difference in the apoptosis rate of CD34+

p-p38

MKK3/6

p-p53

Bcl-xl protein expression in Andriol group before and after treatment. P-p38 protein expression and CD34+ cell apoptosis rate were positively correlated before treatment in control group (P <0.01)

and the decrease in apoptosis rate of CD34+ was positively correlated with decrease in p-p38 protein expression after treatment in FSG group. Conclusion: FSG could inhibit the apoptosis of bone marrow CD34+cells by regulating the p38MAPK pathway

and improve the ineffective hematopoiesis of bone marrow.

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