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在骨关节炎大鼠模型中,电针通过抑制丝裂原活化蛋白激酶来防止关节软骨侵蚀。

Electroacupuncture protects against articular cartilage erosion by inhibiting mitogen-activated protein kinases in a rat model of osteoarthritis.

作者信息

Liao Ying, Li Xinhong, Li Neng, Zhou Jun

机构信息

Department of Rehabilitation, The First Affiliated Hospital of University of South China, Hengyang, Hunan, People's Republic of China.

Hunan Polytechnic of Environment and Biology, Hengyang, Hunan, People's Republic of China.

出版信息

Acupunct Med. 2016 Aug;34(4):290-5. doi: 10.1136/acupmed-2015-010949. Epub 2016 Jan 25.

Abstract

OBJECTIVE

The therapeutic effects of electroacupuncture (EA) on osteoarthritis (OA) are well documented; however, the precise mechanisms of action have not yet been fully elucidated. The present study aimed to investigate the effect of EA on cartilage in an experimental animal model of OA induced by anterior cruciate ligament transection (ACLT) and to examine for concomitant changes in the expression of mitogen-activated protein kinases (MAPKs) in the articular cartilage.

METHODS

Thirty-three-month-old male Sprague Dawley rats were randomly divided into the following three groups (n=10 each): sham operated group (Control group), ACLT without treatment (ACLT group), and ACLT with EA treatment (ACLT+EA group). One week after ACLT, rats in the ACLT+EA group received 12 weeks of EA treatment. Histological analysis and quantitative real-time PCR were used to investigate the effects of EA on cartilage morphology (quantified using modified Mankin scores) and expression of MAPKs (p38, c-Jun N-terminal kinase (c-Jun), and extracellular signal-regulated kinase (ERK)1), respectively.

RESULTS

ACLT produced coarse cartilage surfaces, fibrous degeneration, and fissuring, all of which were suppressed by EA treatment. Although Mankin scores in the ACLT+EA group were significantly higher compared to the Control group (p<0.01), they were significantly lower than the (untreated) ACLT group (p<0.01). The increase in mRNA expression of p38, c-Jun, ERK1, and matrix metalloproteinase (MMP)-13 observed in cartilage after ACLT was significantly inhibited by EA.

CONCLUSIONS

EA appears to prevent the degeneration of articular cartilage, at least partly through regulation of MMP-13 and inhibition of MAPKs in the cartilage of rats with ACLT-induced OA.

摘要

目的

电针(EA)对骨关节炎(OA)的治疗效果已有充分记载;然而,其确切作用机制尚未完全阐明。本研究旨在探讨EA对前交叉韧带横断(ACLT)诱导的OA实验动物模型中软骨的影响,并检测关节软骨中丝裂原活化蛋白激酶(MAPKs)表达的伴随变化。

方法

将33月龄雄性Sprague Dawley大鼠随机分为以下三组(每组n = 10):假手术组(对照组)、未治疗的ACLT组(ACLT组)和接受EA治疗的ACLT组(ACLT + EA组)。ACLT术后1周,ACLT + EA组大鼠接受12周的EA治疗。分别采用组织学分析和定量实时PCR研究EA对软骨形态(使用改良Mankin评分进行量化)和MAPKs(p38、c-Jun氨基末端激酶(c-Jun)和细胞外信号调节激酶(ERK)1)表达的影响。

结果

ACLT导致软骨表面粗糙、纤维变性和裂隙形成,而EA治疗可抑制所有这些变化。虽然ACLT + EA组的Mankin评分显著高于对照组(p < 0.

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