J Rheum Dis 2015; 22(2): 85-92
Published online April 30, 2015
© Korean College of Rheumatology
방지혜1ㆍ하은영2,3ㆍ허지안4
계명대학교 의과대학 1내과학교실, 2생화학교실, 3통증연구소, 4영남대학교 의과대학 내과학교실
Correspondence to : Jian Hur
Objective. Rheumatoid arthritis, the most common form of arthritis, is typically characterized by induced inflammatory pain
in joints. Recent studies have reported on the expression of pain receptors such as transient receptor potential vanilloid 1
(TRPV1) and acid sensing ion channel 3 (ASIC3), which are related to pain induction and regulation. This study was conducted
to investigate the expression of TRPV1 and ASIC3 in response to the analgesic effect of an arthritis treatment in a collagen-induced
arthritis (CIA). Methods. Mice were divided into 3 groups: Control, CIA, and CIA with arthritis treatment. Mice received
intraperitoneal injection with 10 mg/kg infliximab and 10 mg/kg meloxicam five times per week for 3 weeks. Mechanical hyperalgesia,
histologic examination of the feet, serum levels of inflammatory cytokine such as interleukin-6 (IL-6), and interleukin-17
(IL-17), TRPV1 and ASIC3 expression were investigated. Results. The serum levels of IL-6 and IL-17 were lower in the treatment
group (73.77±10.11 pg/mL and 26.75±7.17 pg/mL, respectively) compared to the CIA group (p<0.001). Histological analysis
showed decreased synovial cell proliferation, leukocyte infiltration, and cartilage destruction in the treatment group compared
with the CIA group. The CIA group that underwent arthritis treatment showed a significantly increased withdrawal threshold
of mechanical nociception on the hind paw and increased expression of TRPV1 and ASIC3 compared to the CIA group.
Conclusion. Arthritis treatment resulted in an anti-inflammatory and analgesic effect through upregulation of the activity of
TRPV1 and ASIC3 in CIA mice. (J Rheum Dis 2015;22:85-92)
Keywords Rheumatoid arthritis, TRPV1, ASIC3, Inflammatory pain
J Rheum Dis 2015; 22(2): 85-92
Published online April 30, 2015
Copyright © Korean College of Rheumatology.
방지혜1ㆍ하은영2,3ㆍ허지안4
계명대학교 의과대학 1내과학교실, 2생화학교실, 3통증연구소, 4영남대학교 의과대학 내과학교실
Jihye Bang1, Eunyoung Ha2,3, Jian Hur4
Departments of 1Internal Medicine and 2Biochemistry, 3Pain Research Center, Keimyung University School of Medicine, 4Department of Internal Medicine, Yeungnam University College of Medicine, Daegu, Korea
Correspondence to:Jian Hur
Objective. Rheumatoid arthritis, the most common form of arthritis, is typically characterized by induced inflammatory pain
in joints. Recent studies have reported on the expression of pain receptors such as transient receptor potential vanilloid 1
(TRPV1) and acid sensing ion channel 3 (ASIC3), which are related to pain induction and regulation. This study was conducted
to investigate the expression of TRPV1 and ASIC3 in response to the analgesic effect of an arthritis treatment in a collagen-induced
arthritis (CIA). Methods. Mice were divided into 3 groups: Control, CIA, and CIA with arthritis treatment. Mice received
intraperitoneal injection with 10 mg/kg infliximab and 10 mg/kg meloxicam five times per week for 3 weeks. Mechanical hyperalgesia,
histologic examination of the feet, serum levels of inflammatory cytokine such as interleukin-6 (IL-6), and interleukin-17
(IL-17), TRPV1 and ASIC3 expression were investigated. Results. The serum levels of IL-6 and IL-17 were lower in the treatment
group (73.77±10.11 pg/mL and 26.75±7.17 pg/mL, respectively) compared to the CIA group (p<0.001). Histological analysis
showed decreased synovial cell proliferation, leukocyte infiltration, and cartilage destruction in the treatment group compared
with the CIA group. The CIA group that underwent arthritis treatment showed a significantly increased withdrawal threshold
of mechanical nociception on the hind paw and increased expression of TRPV1 and ASIC3 compared to the CIA group.
Conclusion. Arthritis treatment resulted in an anti-inflammatory and analgesic effect through upregulation of the activity of
TRPV1 and ASIC3 in CIA mice. (J Rheum Dis 2015;22:85-92)
Keywords: Rheumatoid arthritis, TRPV1, ASIC3, Inflammatory pain
Byeongzu Ghang, M.D., Ph.D., Jin Kyun Park, M.D., Ph.D., Ji Hyeon Ju, M.D., Ph.D., Seungwoo Han, M.D., Ph.D.
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J Rheum Dis -0001; ():Soo Min Ahn, M.D., Ph.D., Seonok Kim, MSc., Ye-Jee Kim, Ph.D., Seokchan Hong, M.D., Ph.D., Chang-Keun Lee, M.D., Ph.D., Bin Yoo, M.D., Ph.D., Ji Seon Oh, M.D., Ph.D., Yong-Gil Kim, M.D., Ph.D.
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