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补肾强脊颗粒含药血清通过体外抑制BMP/Smads信号通路抑制强直性脊柱炎中成纤维细胞的成骨分化。

Bushen Qiangji Granule () medicated serum inhibits osteogenic differentiation of fibroblasts in ankylosing spondylitis by inhibiting the BMP/Smads signal pathway in vitro.

作者信息

Liu Hong-Xiao, Jiang Nan, Liang Hui-Ying, Zhou Ying-Yan, Feng Xing-Hua, Feng Xiao-Yan, Zhang He-Qiu, Wu Zhi-Kui, Jiang Quan, Fu Jiao, Ma Xiao-Juan, Chen Peng

机构信息

Department of Rheumatology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.

Department of Vaccine Engineering, Beijing Institute of Basic Medical Sciences, Beijing, 100850, China.

出版信息

Chin J Integr Med. 2016 Nov;22(11):817-822. doi: 10.1007/s11655-016-2268-9. Epub 2016 Oct 26.

Abstract

OBJECTIVE

To explore the mechanism of Bushen Qiangji Granule (, BSQJ) in restraining the osteogenic differentiation of ankylosing spondylitis (AS) fifibroblasts.

METHODS

Hip joint capsules were obtained from AS patients (n=10) receiving total hip replacement and healthy hip joint capsules from patients with hip fracture (n=10) receiving surgery as a control. Finite fifibroblast lines were established from these tissue samples to observe the effect of BSQJ on suppressing osteogenic differentiation of fifibroblasts. The expression of osteogenic marker gene corebinding factor a1 (Cbfa1) and Smad family proteins were examined by Western blot and real-time quantitative polymerase chain reaction (qPCR).

RESULTS

The mRNA expression level of Cbfa1 was significantly higher in AS fibroblasts than that in normal fibroblasts and the expression of pSmad1, pSmad5, Smad4 and Cbfa1 in AS fibroblasts was also higher, demonstrating the activation of the BMP/Smads signal pathway in AS fifibroblasts. BSQJ-medicated serum not only restrained the mRNA and protein expression levels of Cbfa1 and inhibited protein expression level of Smad4 but also decreased the expression quantities of pSmad1 and pSmad5.

CONCLUSIONS

BSQJ can inhibit osteogenic differentiation of AS fifibroblasts in vitro by suppressing the activation of the BMP/Smads signal pathway. This may be the important molecular mechanism of BSQJ in regulating AS ossifification.

摘要

目的

探讨补肾强脊颗粒(BSQJ)抑制强直性脊柱炎(AS)成纤维细胞成骨分化的机制。

方法

取接受全髋关节置换术的AS患者(n = 10)的髋关节囊和接受手术的髋部骨折患者(n = 10)的健康髋关节囊作为对照。从这些组织样本中建立有限的成纤维细胞系,以观察BSQJ对抑制成纤维细胞成骨分化的作用。通过蛋白质免疫印迹法和实时定量聚合酶链反应(qPCR)检测成骨标志物基因核心结合因子a1(Cbfa1)和Smad家族蛋白的表达。

结果

AS成纤维细胞中Cbfa1的mRNA表达水平显著高于正常成纤维细胞,且AS成纤维细胞中pSmad1、pSmad5、Smad4和Cbfa1的表达也较高,表明AS成纤维细胞中BMP/Smads信号通路被激活。BSQJ含药血清不仅抑制Cbfa1的mRNA和蛋白表达水平,抑制Smad4的蛋白表达水平,还降低pSmad1和pSmad5的表达量。

结论

BSQJ可通过抑制BMP/Smads信号通路的激活在体外抑制AS成纤维细胞的成骨分化。这可能是BSQJ调节AS骨化的重要分子机制。

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