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Korean J Physiol Pharmacol. 2016 Jan;20(1):129-36. doi: 10.4196/kjpp.2016.20.1.129. Epub 2015 Dec 31.

The effects of intra-articular resiniferatoxin on monosodium iodoacetate-induced osteoarthritic pain in rats.

Author information

1
Neuroscience Research Institute and Department of Physiology, Korea University College of Medicine, Seoul 02841, Korea.; Rehabilitation Science Program, Department of Public Health Science, Graduate School, Korea University, Seoul 02841, Korea.
2
Rehabilitation Science Program, Department of Public Health Science, Graduate School, Korea University, Seoul 02841, Korea.
3
School of Health and Fitness Management, College of Health and Welfare, Woosong University, Daejeon 34606, Korea.
4
Rehabilitation Science Program, Department of Public Health Science, Graduate School, Korea University, Seoul 02841, Korea.; Department of Rehabilitation Policy and Standardization, National Rehabilitation Research Institute (KNRRI), Seoul 01022, Korea.
5
Rehabilitation Science Program, Department of Public Health Science, Graduate School, Korea University, Seoul 02841, Korea.; Department of Physical Therapy, Korea University College of Health Science, Seoul 02841, Korea.
6
Advanced Biomedical and Welfare Group, Korea Institute of Industrial Technology (KITECH), Cheonan 31056, Korea.
7
Neuroscience Research Institute and Department of Physiology, Korea University College of Medicine, Seoul 02841, Korea.

Abstract

This study was performed to investigate whether an intra-articular injection of transient receptor potential vanilloid 1 (TRPV1) receptor agonist, resiniferatoxin (RTX) would alleviate behavioral signs of arthritic pain in a rat model of osteoarthritis (OA). We also sought to determine the effect of RTX treatment on calcitonin gene-related peptide (CGRP) expression in the spinal cord. Knee joint inflammation was induced by intra-articular injection of monosodium iodoacetate (MIA, 8 mg/50 µl) and weight bearing percentage on right and left hindpaws during walking, paw withdrawal threshold to mechanical stimulation, and paw withdrawal latency to heat were measured to evaluate pain behavior. Intra-articular administration of RTX (0.03, 0.003 and 0.0003%) at 2 weeks after the induction of knee joint inflammation significantly improved reduction of weight bearing on the ipsilateral hindlimb and increased paw withdrawal sensitivity to mechanical and heat stimuli. The reduction of pain behavior persisted for 3~10 days according to each behavioral test. The MIA-induced increase in CGRP immunoreactivity in the spinal cord was decreased by RTX treatment in a dose-dependent manner. The present study demonstrated that a single intra-articular administration of RTX reduced pain behaviors for a relatively long time in an experimental model of OA and could normalize OA-associated changes in peptide expression in the spinal cord.

KEYWORDS:

Calcitonin gene-related peptide (CGRP); Joint pain; Monosodium iodoacetate (MIA); Osteoarthritis; Resiniferatoxin (RTX)

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