| 虎杖苷调节JAK2/STAT3信号通路治疗大鼠激素性股骨头坏死的实验研究 |
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投稿时间：2024-11-18
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| 作者 | Author | 单位 | Address | E-Mail |
| 杨祥军 |
YANG Xiang-jun |
黑龙江中医药大学附属第二医院, 黑龙江 哈尔滨 150001 |
The Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin 150001, Heilongjiang, China |
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| 王丛悦 |
WANG Cong-yue |
哈尔滨市中医医院, 黑龙江 哈尔滨 150070 |
Harbin Hospital of Traditional Chinese Medicine, Harbin 150070, Heilongjiang, China |
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| 徐西林 |
XU Xi-lin |
黑龙江中医药大学附属第三医院, 黑龙江 哈尔滨 150030 |
The Third Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin 150030, Heilongjiang, China |
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| 胡海 |
HU Hai |
黑龙江中医药大学附属第二医院, 黑龙江 哈尔滨 150001 |
The Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin 150001, Heilongjiang, China |
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| 申意伟 |
SHEN Yi-wei |
黑龙江中医药大学附属第二医院, 黑龙江 哈尔滨 150001
天津中医药大学第四附属医院, 天津 300451 |
The Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin 150001, Heilongjiang, China
The Fourth Affiliated Hospital of Tianjin University of Chinese Medicine, Tianjin 300451, China |
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| 张晓峰 |
ZHANG Xiao-feng |
黑龙江中医药大学附属第二医院, 黑龙江 哈尔滨 150001 |
The Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin 150001, Heilongjiang, China |
zxfeng@163.com |
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| 期刊信息：《中国骨伤》2025年，第38卷，第2期，第195-203页 |
| DOI：10.12200/j.issn.1003-0034.20240924 |
| 基金项目:黑龙江省中医药科研项目(编号:2023327) |
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中文摘要:
目的: 探讨虎杖苷对大鼠激素性股骨头坏死(steroid-induced osteonecrosis of the femoral head,SONFH)的治疗效果及其通过调节Janus激酶2/信号转导和转录激活因子3信号通路(janus kinase 2/signal transducer and activator of transcription 3 signaling pathway,JAK2/STAT3)影响骨组织保护的潜在机制。
方法: 5周雄性SD大鼠50只随机分为对照组、模型组、虎杖苷低剂量组(虎杖苷-L)、虎杖苷高剂量组(虎杖苷-H)及虎杖苷-H+Colivelin(JAK2/STAT3通路激活剂)组,每组10只。通过脂多糖和醋酸泼尼松龙诱导SONFH模型。治疗组在模型组基础上每日分别灌胃给予虎杖苷-L 10 mg·kg-1,虎杖苷-H 20 mg·kg-1,虎杖苷-H+Colivelin组腹腔注射Colivelin 1 mg·kg-1,对照组和模型组给予等体积生理盐水,持续6周。观察指标包括血清钙(calcium,Ca)、血清磷(phosphorus,P)、碱性磷酸酶(alkaline phosphatase,ALP)及转化生长因子β1(transforming growth factor β1,TGF-β1)水平,micro-CT扫描,苏木精-伊红染色及Western blot检测JAK2/STAT3信号通路和成骨分化标志基因Runt相关转录因子2(runt-related transcription factor 2,Runx2)、骨形态发生蛋白2(bone morphogenetic protein 2,BMP2)、骨桥蛋白(osteopontin,OPN)蛋白表达。
结果: 与模型组相比,虎杖苷-L和虎杖苷-H组大鼠骨小梁面积百分比显著提升,空骨陷窝率显著下降(P<0.05)。Micro-CT分析表明,虎杖苷处理组骨体积分数、骨小梁数量和厚度增加,骨小梁分离度降低(P<0.05)。血清生化指标检测发现,虎杖苷-L和虎杖苷-H组大鼠血清Ca、P浓度恢复,碱性磷酸酶水平降低,转化生长因子β1水平升高(P<0.05)。Western blot分析显示,虎杖苷显著抑制了模型组中JAK2/STAT3信号通路的激活,同时促进了Runx2、BMP2、OPN等成骨分化标志基因的表达(P<0.05)。与虎杖苷-H组相比,虎杖苷-H+Colivelin组的这些改善效果有所减弱,显示JAK2/STAT3信号通路在虎杖苷作用中的重要性。
结论: 虎杖苷通过调节JAK2/STAT3信号通路,促进成骨分化,改善骨微观结构,对大鼠SONFH具有显著的治疗效果。 |
| 【关键词】虎杖苷 JAK2/STAT3信号通路 激素性股骨头坏死 成骨分化 骨组织保护 |
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| Regulation of JAK2/STAT3 signaling pathway by polydatin in the treatment of hormone-induced femoral head necrosis in rats |
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ABSTRACT
Objective To explore the therapeutic effect of polygonum cuspidatum glycoside on steroid-induced osteonecrosis of the femoral head(SONFH) in rats and its potential mechanism of protecting bone tissue by regulating the Janus kinase 2/signal transducer and activator of transcription 3 signaling pathway(JAK2/STAT3).
Methods Fifty male SD rats were randomly divided into control group,model group,low-dose polygonum cuspidatum glycoside group (polygonum cuspidatum glycoside-L),high-dose polygonum cuspidatum glycoside group (polygonum cuspidatum glycoside-H),and polygonum cuspidatum glycoside-H+Colivelin (JAK2/STAT3 pathway activator) group. SONFH model was induced by lipopolysaccharide and dexamethasone. The treatment groups were given polygonum cuspidatum glycoside orally(polygonum cuspidatum glycoside-L 10 mg·kg-1,polygonum cuspidatum glycoside-H 20 mg·kg-1,and the polygonum cuspidatum glycoside-H+Colivelin group was injected with Colivelin (1 mg·kg-1) intraperitoneally once a day,while the control and model groups were given an equal volume of saline for 6 weeks. The observed indicators included serum calcium(Ca),serum phosphorus (P),alkaline phosphatase,and transforming growth factor β1(TGF-β1) levels,micro-CT scanning,hematoxylin-eosin staining,and Western blot detection of JAK2/STAT3 signaling pathway and osteogenic differentiation marker genes,including Runt-related transcription factor 2 (Runx2),bone morphogenetic protein 2 (BMP2),and osteopontin (OPN) protein expression.
Results Compared with the model group,the trabecular bone area percentage in the polygonum cuspidatum glycoside-L and polygonum cuspidatum glycoside-H groups was significantly increased,and the empty lacunar rate was significantly decreased (P<0.05). Micro-CT analysis showed that the bone volume fraction,trabecular number,and thickness increased,and the trabecular separation decreased in the polygonum cuspidatum glycoside-treated groups(P<0.05). Serum biochemical tests found that the serum Ca and P concentrations in the polygonum cuspidatum glycoside-L and polygonum cuspidatum glycoside-H groups were restored,the alkaline phosphatase levels decreased,and the transforming growth factor β1 levels increased (P<0.05). Western blot analysis showed that polygonum cuspidatum glycoside significantly inhibited the activation of the JAK2/STAT3 signaling pathway in the model group and promoted the expression of osteogenic differentiation marker genes such as Runx2,BMP2,and OPN (P<0.05). Compared with the polygonum cuspidatum glycoside-H group,the improvements in the polygonum cuspidatum glycoside-H+Colivelin group were somewhat weakened,indicating the importance of the JAK2/STAT3 signaling pathway in the action of polygonum cuspidatum glycoside.
Conclusion polygonum cuspidatum glycoside promotes osteogenic differentiation,improves bone microstructure,and has significant therapeutic effects on rat SONFH by regulating the JAK2/STAT3 signaling pathway. |
| KEY WORDS Polygonum cuspidatum glycoside JAK2/STAT3 signaling pathway Steroid-induced osteonecrosis of the femoral head Osteogenic differentiation Bone tissue protection |
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| 引用本文，请按以下格式著录参考文献： |
| 中文格式: | 杨祥军,王丛悦,徐西林,胡海,申意伟,张晓峰.虎杖苷调节JAK2/STAT3信号通路治疗大鼠激素性股骨头坏死的实验研究[J].中国骨伤,2025,38(2):195~203 |
| 英文格式: | YANG Xiang-jun,WANG Cong-yue,XU Xi-lin,HU Hai,SHEN Yi-wei,ZHANG Xiao-feng.Regulation of JAK2/STAT3 signaling pathway by polydatin in the treatment of hormone-induced femoral head necrosis in rats[J].zhongguo gu shang / China J Orthop Trauma ,2025,38(2):195~203 |
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