Acupuncture reduces pain in rats with osteoarthritis by inhibiting MCP2/CCR2 signaling pathway

Author:

Li Bocun1ORCID,Jing Li1,Jia Li2,Qian Tan1,Jianyi Chen2,Zhongsheng Huang2,Xiaohong Zhou2,Guowei Cai1

Affiliation:

1. Department of Acupuncture, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

2. College of Acupuncture and Orthopedics, Hubei University of Chinese Medicine/Hubei Provincial Collaborative Innovation Center of Preventive Treatment by Acupuncture and Moxibustion, Wuhan 430061, China

Abstract

Acupuncture is an emerging alternative therapy that has been beneficial for the pain of osteoarthritis (OA). However, the underlying mechanism of protective effect remains unclear. MCP1/CCR2 axis can be stimulated in various periods of OA, and we hypothesize that acupuncture may treat OA by regulating the MCP1/CCR2 axis. This study aimed to explore the effect of acupuncture at points ST35 and ST36 on the effects of hyperalgesia and cartilage in OA rats including the expression of chemokines, nerve growth factor (NGF), and inflammatory-related proteins. OA was induced in male Sprague–Dawley rats by anterior cruciate ligament transection at the right knee. The first acupuncture intervention was performed on the seventh day after surgery and once a day for seven weeks. The knee-pain-related behaviors, histology, and related protein were examined in this study. We have found that electroacupuncture at ST35 and ST36 can significantly alleviate the hyperalgesia and cartilage degeneration as well as reducing nerve sprouting in OA knee joint. Moreover, acupuncture treatment may inhibit the MCP1/CCR2 axis as well as down-regulate inflaming factor and NGF in cartilage and synovial tissue. The data presented here indicate that acupuncture exerts a protective effect against hyperalgesia and cartilage degeneration, and the mechanism might involve in chemokines and NGF pathway.

Funder

National Natural Science Foundation of China

Hubei Provincial Health Committee

Publisher

SAGE Publications

Subject

General Biochemistry, Genetics and Molecular Biology

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