Analgesic effects of NB001 on mouse models of arthralgia.

Zhen Tian,Ming-Gao Zhao,Xin-Shang Wang,Jing Han,Bin Feng,Nan Zhang,Yan-Yan Guo,Dong-Sheng Wang,Jiao Tian,Shui-Bing Liu

doi:10.1186/s13041-015-0151-9

Abstract

Our previous studies have demonstrated the critical roles of calcium-stimulated adenylyl cyclase 1 (AC1) in the central nervous system in chronic pain. In the present study, we examined the analgesic effects of NB001, a selective inhibitor of AC1, on animal models of ankle joint arthritis and knee joint arthritis induced by complete Freund’s adjuvant injection. NB001 treatment had no effect on joint edema, stiffness, and joint destruction. Furthermore, the treatment failed to attenuate the disease progression of arthritis. However, NB001 treatment (3 mg/kg) significantly weakened joint pain-related behavior in the mouse models of ankle joint arthritis and knee joint arthritis. Results indicated that NB001 exhibited an analgesic effect on the animal models of arthritis but was not caused by anti-inflammatory activities.

Highlights

Arthritis is the most common musculoskeletal disease and is characterized by joint inflammation, stiffness, pain, and cartilage damage [1]
We aimed to examine the analgesic effect of NB001 on the (i) ankle joint pain induced by injecting complete Freund’s adjuvant (CFA) into the hind metatarsal footpad, as well as on the (ii) knee joint pain caused by CFA administration into the knee joint cavity
NB001 exerted no effect on CFA-induced joint inflammation Experimental procedure of two arthritic pain models was sown in the Fig. 1

Summary

Introduction

Arthritis is the most common musculoskeletal disease and is characterized by joint inflammation, stiffness, pain, and cartilage damage [1]. Among these symptoms, arthralgia negatively influences the articular function and quality of life of patients. Chronic arthralgia leads to mobility disorders and physical disability and causes a substantial amount of emotional and economic stress [2, 3]. The mechanism underlying arthritic joint pain is still poorly understood. Non-steroidal anti-inflammatory drugs and opioids have been widely used as therapies in the clinical treatment of arthritic joint pain for decades [4, 5]. The long-term use of both treatments exhibit non-negligible adverse effects

Objectives

Methods

Results