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颈舒颗粒胶囊及其成分对人滑膜细胞MH7A细胞的抗炎作用。

Anti-inflammatory effects of Jingshu Keli capsule and its components on human synoviocyte MH7A cells.

作者信息

Meng Xiangbo, Cheng Wenxiang, Zhong Shan, Zhang Peng, Qin Ling, Wang Xinluan

机构信息

Translational Medicine R&D Center, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.

Musculoskeletal Research Laboratory, Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong, SAR, China.

出版信息

Arthroplasty. 2020 Mar 9;2(1):7. doi: 10.1186/s42836-020-00026-8.

DOI:10.1186/s42836-020-00026-8
PMID:35236422
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8796523/
Abstract

BACKGROUND: Jingshu Keli (JSKL), a traditional Chinese medicine (TCM) formula consisting of multiple active compounds, has been officially approved by National Medical Products Administration (NMPA) for treatment of cervical radiculopathy. It relieves pain, according to TCM theory, by activating blood circulation to dissipate blood stasis. The pain mainly stems from neurogenic inflammation caused by mechanical compression of the cervical nerve root. In addition, inflammation mediators also cause the development of other joint diseases, such as osteoarthritis (OA). The purpose of this paper was to evaluate the anti-inflammatory effects of JSKL and identify the biologically active herbs and compounds in vitro. METHODS: Enzyme-linked immunosorbent assay (Elisa) was used to determine the expression of pro-inflammatory cytokines, tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6) and interleukin 8 (IL-8), in the culture medium of human MH7A cells stimulated by lipopolysaccharides (LPS). RESULTS: JSKL and three single-herb capsules, Cinnamomum cassia Presl (C.C.), Angelica Sinensis (Oliv.) Diels (A.S.) and Carthamus tinctorius L. (C.T.), significantly inhibited the secretion of TNF-α. If one of these three herbal components was removed, suppressing effect of the single-herb-deleted JSKL on TNF-α was abolished. Cinnamaldehyde (CIN) from C.C. was the most potent ingredient that inhibited the expression of IL-6 and IL-8 in the culture medium of both LPS-stimulated MH7A cells and primary synovial cells. CONCLUSIONS: JSKL was found to possess anti-inflammatory effect in vitro; C.C., A.S. and C.T. were the principal and essential herbal components responsible for such activity; CIN from C.C. is one the most potent single compound among indicator components of JSKL recorded in 2015 Chinese pharmacopoeia. This study provided scientific evidence for the clinical application of JSKL as an agent for targeted treatment of cervical radiculopathy. Furthermore, CIN has potential to be used for the treatment of some inflammation-related orthopedic diseases, such as rheumatic arthritis and osteoarthritis.

摘要

背景：颈舒颗粒（JSKL）是一种由多种活性成分组成的中药方剂，已获国家药品监督管理局（NMPA）正式批准用于治疗神经根型颈椎病。根据中医理论，它通过活血化瘀来缓解疼痛。疼痛主要源于颈神经根机械性压迫引起的神经源性炎症。此外，炎症介质也会导致其他关节疾病的发展，如骨关节炎（OA）。本文旨在评估颈舒颗粒的抗炎作用，并在体外鉴定其生物活性草药和化合物。 方法：采用酶联免疫吸附测定（ELISA）法测定脂多糖（LPS）刺激的人MH7A细胞培养基中促炎细胞因子肿瘤坏死因子-α（TNF-α）、白细胞介素6（IL-6）和白细胞介素8（IL-8）的表达。 结果：颈舒颗粒和三种单味药胶囊，即肉桂（C.C.）、当归（A.S.）和红花（C.T.），均显著抑制TNF-α的分泌。若去除这三种草药成分中的一种，去除单味药的颈舒颗粒对TNF-α的抑制作用即消失。肉桂中的肉桂醛（CIN）是抑制LPS刺激的MH7A细胞和原代滑膜细胞培养基中IL-6和IL-8表达的最有效成分。 结论：发现颈舒颗粒在体外具有抗炎作用；肉桂、当归和红花是产生该活性的主要和必需草药成分；肉桂中的肉桂醛是2015年《中国药典》记载的颈舒颗粒指标成分中最有效的单一化合物之一。本研究为颈舒颗粒作为靶向治疗神经根型颈椎病药物的临床应用提供了科学依据。此外，肉桂醛有潜力用于治疗一些与炎症相关的骨科疾病，如风湿性关节炎和骨关节炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/5ffdde77821d/42836_2020_26_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/870980a171d9/42836_2020_26_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/33b1d8603e25/42836_2020_26_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/124c54e8e0e5/42836_2020_26_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/b375d0841479/42836_2020_26_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/316fa93b6af0/42836_2020_26_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/7ebdc4d29339/42836_2020_26_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/5ffdde77821d/42836_2020_26_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/870980a171d9/42836_2020_26_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/33b1d8603e25/42836_2020_26_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/124c54e8e0e5/42836_2020_26_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/b375d0841479/42836_2020_26_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/316fa93b6af0/42836_2020_26_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/7ebdc4d29339/42836_2020_26_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3821/8796523/5ffdde77821d/42836_2020_26_Fig7_HTML.jpg

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本文引用的文献

[1]
Cinnamaldehyde Inhibits Inflammation of Human Synoviocyte Cells Through Regulation of Jak/Stat Pathway and Ameliorates Collagen-Induced Arthritis in Rats.

J Pharmacol Exp Ther. 2020-2-6

[2]
Effects of Zoledronate on Local and Systemic Production of IL-1β, IL-18, and TNF-α in Mice and Augmentation by Lipopolysaccharide.

Biol Pharm Bull. 2019

[3]
Salvianolic acid B remits LPS-induced injury by up-regulating miR-142-3p in MH7A cells.

Biomed Pharmacother. 2019-4-22

[4]
Effects of Ghrelin on the Apoptosis of Rheumatoid Arthritis Fibroblast-Like Synoviocyte MH7A Cells.

Biol Pharm Bull. 2019-2-1

[5]
Informed appropriate imaging for low back pain management: A narrative review.

J Orthop Translat. 2018-8-27

[6]
miR-145 eliminates lipopolysaccharides-induced inflammatory injury in human fibroblast-like synoviocyte MH7A cells.

J Cell Biochem. 2018-9-7

[7]
Involvement of Voltage-Gated Calcium Channels in Inflammation and Inflammatory Pain.

Biol Pharm Bull. 2018

[8]
Steroid-associated osteonecrosis: Epidemiology, pathophysiology, animal model, prevention, and potential treatments (an overview).

J Orthop Translat. 2015-1-13

[9]
The roles of inflammatory mediators and immunocytes in tendinopathy.

J Orthop Translat. 2018-4-14

[10]
Jingshu Keli attenuates cervical spinal nerve ligation-induced allodynia in rats through inhibition of spinal microglia and Stat3 activation.

Spine J. 2018-6-30

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