Effects of Safflower Extract on the Expressions of ERK,JNK and P38 in Femoral Head Tissue of Rabbits With Steroid-Induced Avascular Necrosis

WAN Tian; WU Minrui; QI Zhenxi

doi:10.13288/j.11-2166/r.2013.23.016

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Effects of Safflower Extract on the Expressions of ERK,JNK and P38 in Femoral Head Tissue of Rabbits With Steroid-Induced Avascular Necrosis

更新时间：2021-11-17

- Effects of Safflower Extract on the Expressions of ERK,JNK and P38 in Femoral Head Tissue of Rabbits With Steroid-Induced Avascular Necrosis
- Journal of Traditional Chinese Medicine Vol. 54, Issue 23, Pages: 2039-2042(2013)
- 作者机构：
  
  1. 福建中医药大学骨伤学院
  2. 福建中医药大学中西医结合学院
- 作者简介：
- 基金信息：
- DOI：10.13288/j.11-2166/r.2013.23.016
  CLC： R274;R285.5
- Published：2013
- 稿件说明：
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[1]万甜,吴敏瑞,齐振熙.红花提取物对激素性股骨头缺血坏死兔股骨头组织ERK、JNK和P38蛋白表达的影响[J].中医杂志,2013,54(23):2039-2042.

WAN Tian, WU Minrui, QI Zhenxi. Effects of Safflower Extract on the Expressions of ERK,JNK and P38 in Femoral Head Tissue of Rabbits With Steroid-Induced Avascular Necrosis[J]. Journal of Traditional Chinese Medicine2013, 54(23): 2039-2042.
[1]万甜,吴敏瑞,齐振熙.红花提取物对激素性股骨头缺血坏死兔股骨头组织ERK、JNK和P38蛋白表达的影响[J].中医杂志,2013,54(23):2039-2042. DOI： 10.13288/j.11-2166/r.2013.23.016.

WAN Tian, WU Minrui, QI Zhenxi. Effects of Safflower Extract on the Expressions of ERK,JNK and P38 in Femoral Head Tissue of Rabbits With Steroid-Induced Avascular Necrosis[J]. Journal of Traditional Chinese Medicine2013, 54(23): 2039-2042. DOI： 10.13288/j.11-2166/r.2013.23.016.

摘要

目的探讨红花提取物对激素性股骨头缺血坏死的可能作用机制。方法将40只成年新西兰大白兔随机分为正常对照组、模型对照组、髓芯减压组、生理盐水+髓芯减压组、红花提取物+髓芯减压组

每组8只。除正常对照组外

其余各组建立激素性股骨头坏死模型。造模成功后

正常对照组和模型对照组不予处理

髓芯减压组仅行髓芯减压术

生理盐水+髓芯减压组采用髓芯减压术配合髓腔内注射生理盐水

红花提取物+髓芯减压组采用髓芯减压术配合髓腔内注射羟基红花黄色素A（7.2mg/kg）。1周后处死兔

取出患侧股骨头

采用免疫印迹法检测组织中ERK、JNK和P38蛋白表达。结果与正常对照组比较

模型对照组ERK1和ERK2表达明显降低

JNK和P38表达明显升高（P<0.05）;与模型对照组比较

髓芯减压组、生理盐水+髓芯减压组和红花提取物+髓芯减压组ERK1和ERK2表达明显升高

JNK和P38表达明显降低（P<0.05）;与髓芯减压组比较

红花提取物+髓芯减压组ERK1和ERK2表达升高明显

JNK和P38表达降低明显（P<0.05）。结论红花提取物可通过激活丝裂原活化蛋白激酶（MAPK）相关通路

增高ERK的磷酸化水平

降低JNK和P38的磷酸化水平

促进股骨头髓腔内细胞增殖、分化

抑制其凋亡

从而减轻激素导致股骨头缺血坏死的损伤

促进坏死股骨头的修复。

Abstract

Objective To research the possible mechanism of safflower extract for steroid-induced avascular necrosis.Methods Forty adult New Zealand white rabbits were randomized into the normal control group

model control group

core decompression group

normal saline+core decompression group and safflower extract+core decompression group

with 8in each.The models of steroid-induced avascular necrosis were established in all groups except the normal control group.There was no treatment in the normal control group and model control group after modeling.The core decompression group was given the core decompression.The normal saline+core decompression group was given normal saline and core decompression.The safflower extract+core decompression group was given 7.2mg/kg safflower yellow A and core decompression.The rabbits were sacrificed one week later.The femoral head in the affected side was removed and the expressions of ERK

JNK and P38were detected with Western Blotting.Results Comparing with the normal control group

the expressions of ERK1and ERK2were significantly decreased but the expressions of JNK and P38were significantly increased in the model control group（P<0.05）.Comparing with the model control group

the expressions of ERK1and ERK2 were significantly increased but the expressions of JNK and P38were significantly decreased in the core decompression group

normal saline+core decompression group and safflower extract+ core decompression group（P<0.05）.Comparing with the core decompression group

the expressions of ERK1and ERK2were significantly increased but the expressions of JNK and P38were significantly decreased in the safflower extract+ core decompression group（P<0.05）.Conclusion Safflower extract can reduce the damage and promote the repair of steroid-induced avascular necrosis by activating the mitogen-activated protein kinase pathway

increasing the phosphorylation level of ERK

reducing the phosphorylation levels of JNK and P38and promoting cell proliferation and differentiation and inhibiting cell apoptosis of femoral intramedullary.

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