Abstract
Objective. To investigate the relationship between pain behavior and potassium voltage-gated channel subfamily A member 2 (KCNA2) expression in dorsal root ganglia (DRGs) of rats with osteoarthritis (OA). Methods. Male Sprague-Dawley rats were randomly divided into three groups: blank control group (group C), normal saline group (group S), and group OA. Paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) were measured one day before injection and one, two, four, and six weeks after injection. At one, two, four, and six weeks after injection, pathological knee joint changes and activated transcription factor-3 (ATF-3) and KCNA2 expressions in DRGs were analyzed. Results. Compared with preinjection, PWMT and PWTL at two, four, and six weeks after injection were significantly decreased in the group OA (P<0.05 or 0.01). Compared with group C, PWMT and PWTL at two, four, and six weeks after injection were significantly decreased in the group OA (P<0.05 or 0.01). In the group OA, slight local articular cartilage surface destruction was found at week one. The cartilage surface destruction gradually developed, and the exacerbation of cartilage matrix reduction and bone hyperplasia were increasingly aggravated and eventually evolved into advanced OA in the second to sixth weeks. Compared with group C, ATF-3 expression was significantly increased, and KCNA2 expression was significantly decreased in the group OA at two, four, and six weeks after injection (P<0.05 or 0.01). Compared to baseline, ATF-3 expression was significantly increased, and KCNA2 expression was significantly decreased in the group OA (P<0.05 or 0.01). Conclusion. Pain behavior in OA rats was associated with decreased KCNA2 expression in DRGs.
Highlights
OA is a common disease in the aging population which affects bones and motor system; its incidence rate in people who are 65 years old and above is more than 50%, and its prevalence rate in people who are 75 years old and above is approximately 80% [1]
Paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) were significantly lower in the group OA (P < 0.05 or 0.01) at two, four, and six weeks after intra-articular injection; PWMT and PWTL were lowest at four weeks (P < 0.01). ere was no significant difference in PWMT and PWTL between four and six weeks after OA model establishment (P > 0.05)
Compared with group C, at two, four, and six weeks, PWMT and PWTL were significantly decreased in the group OA (P < 0.05 or 0.01)
Summary
OA is a common disease in the aging population which affects bones and motor system; its incidence rate in people who are 65 years old and above is more than 50%, and its prevalence rate in people who are 75 years old and above is approximately 80% [1]. Little is known about the pathogenesis of OA pain, and there is a lack of targeted treatment and measures to control OA pain. Nonsteroidal anti-inflammatory drugs [3, 4] and opioids [5, 6] have a certain effect on relieving OA pain, but longterm use of these drugs has great side effects, and they cannot fundamentally reverse or delay the progression of the disease [7,8,9,10]. Erefore, studying the pathogenesis of OA pain and exploring the possible targets for prevention and treatment of OA pain have a great research value and clinical significance. Increased excitability of neurons in DRGs caused by injury is an important mechanism of chronic pain. Increased excitability of neurons in DRGs caused by injury is an important mechanism of chronic pain. e results of some researches [14,15,16] have confirmed that OA pain has similar characteristics as neuropathic pain (NP), but whether the mechanism of OA
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