Protective effects of Shensuitongzhi formula on intervertebral disc degeneration via downregulation of NF-κB signaling pathway and inflammatory response

被引:2
|
作者
Wang, Xu [1 ,2 ]
Zeng, Qinghe [1 ,2 ]
Ge, Qinwen [1 ,2 ]
Hu, Songfeng [1 ,2 ,3 ]
Jin, Hongting [1 ]
Wang, Ping-er [1 ]
Li, Ju [1 ,4 ]
机构
[1] Zhejiang Chinese Med Univ, Affiliated Hosp 1, Zhejiang Prov Hosp Chinese Med, Inst Orthoped & Traumatol, Hangzhou 310006, Peoples R China
[2] Zhejiang Chinese Med Univ, Coll Clin Med 1, Hangzhou 310053, Peoples R China
[3] Shaoxing Hosp Tradit Chinese Med, Dept Orthopaed & Traumatol, Shaoxing 312000, Zhejiang, Peoples R China
[4] Zhejiang Chinese Med Univ, Affiliated Hosp 1, Dept Orthopaed Surg, Hangzhou 310006, Peoples R China
关键词
Intervertebral disc degeneration; Shensuitongzhi formula; Lumbar spine instability surgery; Cartilage endplate calcification; NF-kappa B signaling pathway; MATRIX METALLOPROTEINASES; LUMBAR FUSION; PAIN; INSIGHTS;
D O I
10.1186/s13018-023-04391-3
中图分类号
R826.8 [整形外科学]; R782.2 [口腔颌面部整形外科学]; R726.2 [小儿整形外科学]; R62 [整形外科学(修复外科学)];
学科分类号
摘要
Low back pain (LBP) is a common orthopedic disease over the world. Lumbar intervertebral disc degeneration (IDD) is regarded as an important cause of LBP. Shensuitongzhi formula (SSTZF) is a drug used in clinical treatment for orthopedic diseases. It has been found that SSTZF can have a good treatment for IDD. But the exact mechanism has not been clarified. The results showed that SSTZF protects against LSI-induced degeneration of cartilage endplates and intervertebral discs. Meanwhile, SSTZF treatment dramatically reduces the expression of inflammatory factor as well as the expression of catabolism protein and upregulates the expression of anabolism protein in LSI-induced mice. In addition, SSTZF delayed the progression of LSI-induced IDD via downregulation the level of NF-kappa B signaling key gene RELA and phosphorylation of key protein P65 in endplate chondrocytes. Our study has illustrated the treatment as well as the latent mechanism of SSTZF in IDD.
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页数:12
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