[1]李冬,董晓俊,余江琴.骨蚀丸通过胰岛素样生长因子1治疗激素性股骨头坏死的机制[J].中国中医骨伤科杂志,2023,31(09):15-18+26.[doi:10.20085/j.cnki.issn1005-0205.230903 ]
　LI Dong,DONG Xiaojun,YU Jiangqin.Effects of Gushi Pills on the Treatment of Steroid-Induced Avascular Necrosis of the Femoral Head in Rabbits Through IGF-1 Pahway[J].Chinese Journal of Traditional Medical Traumatology & Orthopedics,2023,31(09):15-18+26.[doi:10.20085/j.cnki.issn1005-0205.230903 ]
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骨蚀丸通过胰岛素样生长因子1治疗激素性股骨头坏死的机制()
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《中国中医骨伤科杂志》[ISSN:1005-0205/CN:42-1340/R]

卷:
第31卷
期数:
2023年09期
页码:
15-18+26
栏目:
实验研究
出版日期:
2023-09-15

文章信息/Info

Title:
Effects of Gushi Pills on the Treatment of Steroid-Induced Avascular Necrosis of the Femoral Head in Rabbits Through IGF-1 Pahway
文章编号:
1005-0205(2023)09-0015-04
作者:
李冬1; 董晓俊1; 余江琴1
1武汉市中医医院(武汉,430014)
Author(s):
LI Dong1; DONG Xiaojun1; YU Jiangqin1
1Wuhan Hospital of Traditional Chinese Medicine,Wuhan 430014,China.
关键词:
骨蚀丸;  股骨头髓芯减压术;  胰岛素样生长因子1;  激素性股骨头坏死
Keywords:
bone erosion pill;  femoral head medullary core decompression;  insulin-like growth factor 1;  hormonal femoral head necrosis
分类号:
R681.8
DOI:
10.20085/j.cnki.issn1005-0205.230903
文献标志码:
A
摘要:
目的:研究骨蚀丸(Gushi Pills,GSP)通过胰岛素样生长因子1(Insulin-like Growth Factor-1,IGF-1)治疗激素性股骨头坏死(Steroid-induced Necrosis of the Femoral Head,SNOFH)的机制。方法:建立激素性股骨头坏死新西兰兔模型,检测灌服骨蚀丸混悬液对激素性股骨头坏死新西兰兔模型血清的IGF-1水平的影响; 建立激素性股骨头坏死新西兰兔模型,检测股骨头髓芯减压术联合骨蚀丸对成骨早期标志物碱性磷酸酶(Alkaline Phosphatase,ALP)活性和骨钙素含量的影响; 检测骨蚀丸对小鼠间充质干细胞蛋白激酶p38MAPK、ERK和JNK的磷酸化的影响,并检测其对成骨早期标志物碱性磷酸酶的影响。结果:已成功建立激素性股骨头坏死新西兰兔模型。随着灌服骨蚀丸混悬液浓度的升高,模型组血清的IGF-1水平显著升高(P<0.01)。股骨头髓芯减压术组碱性磷酸酶和骨钙素含量显著高于模型组(P<0.01)。股骨头髓芯减压联合骨蚀丸组碱性磷酸酶和骨钙素含量显著高于模型组和股骨头髓芯减压术组(P<0.01)。骨蚀丸干预小鼠间充质干细胞后,p38MAPK、ERK和JNK的磷酸化水平显著升高(P<0.01); 使用SB203580和PD98059分别抑制p38MAPK和ERK活性后,碱性磷酸酶水平均显著降低(P<0.01)。结论:骨蚀丸混悬液灌服可以提高激素性股骨头坏死新西兰兔模型血清的IGF-1水平。通过与股骨头髓芯减压术联合,可以进一步提高激素性股骨头坏死新西兰兔模型的碱性磷酸酶和骨钙素含量。细胞实验的结果显示骨蚀丸可通过激活MAPK信号通路的蛋白激酶p38MAPK、ERK和JNK磷酸化水平治疗激素性股骨头坏死。
Abstract:
Objective:To investigate the mechanism of gushi pills(GSP)on the treatment of steroid-induced necrosis of the femoral head(SNOFH)through insulin-like growth factor-1(IGF-1)pathway.Methods:A New Zealand rabbit model of SNOFH was established,and the effect of GSP infusion on IGF-1 levels in the serum of New Zealand rabbits with SNOFH was examined.A New Zealand rabbit model of SNOFH was established,and the effects of femoral medullary core decompression combined with GSP on the activity of Alkaline phosphatase(ALP)and the content of osteocalcin in early osteogenesis were detected.The effect of GSP on the phosphorylation of p38MAPK,ERK and JNK in mouse mesenchymal stem cells and its effect on the early osteogenic marker ALP were detected.Results:A New Zealand rabbit model of SNOFH has been successfully established.Serum levels of IGF-1 in the model group increased significantly(P<0.01),with increasing concentrations of the infused GSP suspension.The ALP and osteocalcin levels were significantly higher in the femoral head medullary core decompression group than that in the model group(P<0.01).The levels of ALP and osteocalcin were significantly higher in the femoral medullary core decompression combined with GSP group than that in the model and femoral medullary core decompression groups(P<0.01).The p38MAPK,ERK and JNK phosphorylation levels were significantly increased after GSP intervention in mouse MSCs group(P<0.01),the levels of ALP were significantly increased after the inhibition of p38MAPK and ERK by SB203580 and PD98059,respectively.ERK activity were significantly reduced after the inhibition of the p38MAPK and ERK by SB203580 and PD98059,respectively(P<0.01).Conclusion:GSP suspension infusion can increase IGF-1 levels in serum of the SNOFH New Zealand rabbit model.By combining with femoral head medullary core decompression,ALP and osteocalcin levels in the New Zealand rabbit model of SNOFH could be further increased.The results of the cellular assay showed that GSP could treat SNOFH by activating the protein kinase p38MAPK,ERK and JNK phosphorylation levels of the MAPK signaling pathway.

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备注/Memo

备注/Memo:
基金项目:2020年度武汉市临床医学科研项目(WZ20D09)
更新日期/Last Update: 2023-09-01