• Title/Summary/Keyword: Inflammatory pain

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Anti-Arthritic and Analgesic Effect of NDI10218, a Standardized Extract of Terminalia chebula, on Arthritis and Pain Model

  • Seo, Jong-Bae;Jeong, Jae-Yeon;Park, Jae-Young;Jun, Eun-Mi;Lee, Sang-Ik;Choe, Sung-Sik;Park, Do-Yang;Choi, Eun-Wook;Seen, Dong-Seung;Lim, Jong-Soon;Lee, Tae-Gyu
    • Biomolecules & Therapeutics
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    • v.20 no.1
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    • pp.104-112
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    • 2012
  • The fruit of Terminalia chebula Retzius has been used as a panacea in India and Southeast Asia but its biological activities have not been fully elucidated. Here we report anti-arthritic and analgesic effect of NDI10218, a standardized ethanol extract of Terminalia chebula, on collagen-induced arthritis and acetic acid-induced writhing model, respectively. Arthritis was induced in DBA/1J mice by immunizing bovine type II collagen and mice were treated with NDI10218 daily for 5 weeks after the onset of the disease. NDI10218 reduced the arthritis index and blocked the synovial hyperplasia in a dose-dependent manner. The serum levels of pro-inflammatory cytokines TNF-${\alpha}$, IL-6, and IL-$1{\beta}$ were significantly reduced in mice treated with NDI10218. Production of the inflammatory IL-17, but not immunosuppressive IL-10, was also inhibited in splenocytes isolated from NDI10218-treated arthritis mice. Administration of NDI10218 markedly decreased the number of T cell subpopulations in the regional lymph nodes of the arthritis mice. Finally, NDI10218 reduced the number of abdominal contractions in acetic acid-induced writhing model, suggesting an analgesic effect of this extract. Taken together, these results suggest that NDI10218 can be a new therapeutic candidate for the treatment of rheumatoid arthritis.

The Clinical Study One Pelvic Inflammatory Disease (PID) Patient Treatments by Korean Medicine (골반염 환자에 대한 한방치료 치험 1례)

  • Song, Yu-Rim;Kim, Ji-Uun;Yang, Seung-Jeong;Park, Kyung-Mi;Jung, Su-Jung;Cho, Seong-Hee
    • The Journal of Korean Obstetrics and Gynecology
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    • v.27 no.3
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    • pp.158-167
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    • 2014
  • Objectives: This study aims to report the effect of Korean medicine treatments on a pelvic inflammatory disease (PID). Methods: The patient was treated with Qingbaozhuyu-tang, acupuncture at Jungwan (CV12), Gihae (CV6), Taechung (LR3), Hapgok (LI4), Sameumgyo (SP6), Sangryo (BL3), Charyou (BL32), Jungryo (BL33), Haryo (BL34), Cheonchu (ST25), Pungryung (ST40), Duyu (ST8), Taeyang (EX-HN5). And we evaluated treatment effects by visual analogue scale (VAS) and Urine analysis (UA) Finding. Results: After treatments, the symptoms such as lower abdominal pain, pelvic pain and fever were improved and there were no abnormal findings in urine analysis. Conclusions: This study suggests that Korean medicine treatments show effective on PID treatment.

Improvement Effect of Soyeom Pharmacopuncture on Gout via NLRP3 Inflammasome Regulation

  • Sung Wook Kim;Jun Ho Lee;Hyeonjin Kim;Seong Hoon Lee;Dajeong Jeong;Hyuk Soon Kim;Cheol-Jung Lee;Dae Yong Kim;Tae Han Yook;Gabsik Yang
    • Journal of Pharmacopuncture
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    • v.25 no.4
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    • pp.396-403
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    • 2022
  • Objectives: Gout is an inflammatory arthritis of the joints and soft tissues occurring due to deposition of monosodium urate (MSU) crystals, which are caused by persistent hyperuricemia. Soyeom pharmacopuncture is one treatment method that has been traditionally used for pain management in Oriental medicine. However, studies on its effect in reducing gout pain have been insufficient. Therefore, we selected Soyeom pharmacopuncture among natural products used in Korea as the new target of our study. Methods: The effects of Soyeom pharmacopuncture were examined in mouse models of acute gout induced by injection of MSU crystals into footpads. IL-1β, IL-6, and TNF-α production were examined by immunoblotting and enzyme-linked immunosorbent assay as hallmarks of NLRP3 inflammasome and cytokine activation. Results: Soyeom pharmacopuncture reduced foot edema in gout-induced mice, as well as IL-1β, nitrite, IL-6, and TNF-α production. Moreover, Soyeom pharmacopuncture also reduced MSU-induced gout inflammatory gene expressions, specifically those in the NF-kB pathway. Conclusion: Pharmacopuncture may serve as a new solution for other inflammatory diseases as well. Through active follow-up studies, we could thoroughly understand the clinical value of Soyeom pharmacopuncture.

The effects of Honey Bee Venom for Aqua-acupuncture on Expression of Genes Related with Inflammation and Pain (봉독(蜂毒) 약침액(藥鍼液)이 염증(炎症) 및 통증(痛症) 관련(關聯) 유전자(遺傳子) 발현(發現)에 미치는 영향(影響))

  • Jeong, Hye-Yoon;Koh, Hyung-Kyun
    • Journal of Acupuncture Research
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    • v.19 no.3
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    • pp.41-50
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    • 2002
  • Objective : To study anti-inflammatory, analgesic effect and molecular biological mechanism of honey bee venom for aqua-acupuncture, human mast cell line(HMC-1) and human glioma cell line(HS683) were treated with bee venom. Methods : Cell viability of bee venom was tested by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) asssay. To explore whether anti-inflammatory, analgesic effects of bee venom are associated with the control of gene expression, quantitative RT-PCR analysis of inflammation and pain related genes was performed. Results : The MTT assay demonstrated that cell viability was not decreased by treatment with 10-9 ug/ml bee venom in comparison with 10-2, 10-3, 10-4, 10-5, 10-6, 10-7, 10-8, 10-9, 10-10 and 10-11 ug/ml. sPLA2 and COX-l were down-regulated by treatment with 10-9 ug/ml bee venom in HS683 Cell line in comparison with control. COX-2 was up-regulated by treatment with 10-9 ug/ml bee venom in HS683 Cell line and HSP-2 was up-regulated by treatment with 10-9 ug/ml bee venom in HMC-1 Cell line in comparison with control. sPLA2, COX-1 and COX-2 showed no significant regulation in HMC-1 Cell line and cPLA2 also showed no significant regulation in both HMC-l and HS683 Cell line between control and bee venom treated group.

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Participation of central GABAA receptors in the trigeminal processing of mechanical allodynia in rats

  • Kim, Min Ji;Park, Young Hong;Yang, Kui Ye;Ju, Jin Sook;Bae, Yong Chul;Han, Seong Kyu;Ahn, Dong Kuk
    • The Korean Journal of Physiology and Pharmacology
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    • v.21 no.1
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    • pp.65-74
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    • 2017
  • Here we investigated the central processing mechanisms of mechanical allodynia and found a direct excitatory link with low-threshold input to nociceptive neurons. Experiments were performed on male Sprague-Dawley rats weighing 230-280 g. Subcutaneous injection of interleukin 1 beta ($IL-1{\beta}$) ($1ng/10{\mu}L$) was used to produce mechanical allodynia and thermal hyperalgesia. Intracisternal administration of bicuculline, a gamma aminobutyric acid A ($GABA_A$) receptor antagonist, produced mechanical allodynia in the orofacial area under normal conditions. However, intracisternal administration of bicuculline (50 ng) produced a paradoxical anti-allodynic effect under inflammatory pain conditions. Pretreatment with resiniferatoxin (RTX), which depletes capsaicin receptor protein in primary afferent fibers, did not alter the paradoxical anti-allodynic effects produced by the intracisternal injection of bicuculline. Intracisternal injection of bumetanide, an Na-K-Cl cotransporter (NKCC 1) inhibitor, reversed the $IL-1{\beta}$-induced mechanical allodynia. In the control group, application of GABA ($100{\mu}M$) or muscimol ($3{\mu}M$) led to membrane hyperpolarization in gramicidin perforated current clamp mode. However, in some neurons, application of GABA or muscimol led to membrane depolarization in the $IL-1{\beta}$-treated rats. These results suggest that some large myelinated $A{\beta}$ fibers gain access to the nociceptive system and elicit pain sensation via $GABA_A$ receptors under inflammatory pain conditions.

Compression of The Trigeminal Ganglion Enhances Nociceptive Behavior Produced by Formalin in The Orofacial Area of Rats

  • Yang, Gwi-Y.;Park, Young-H.;Lee, Min-K.;Kim, Sung-K.;Ahn, Dong K.
    • International Journal of Oral Biology
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    • v.33 no.4
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    • pp.155-162
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    • 2008
  • The present study investigated inflammatory hypersensitivity following compression of the trigeminal ganglion in rats. Experiments were carried out on male Sprague-Dawley rats weighing 250-260 g. Under anesthesia, rats were mounted on a stereotaxic frame and injected with $8{\mu}L$ of 4% agar solution through a stainless steel injector to compress the trigeminal ganglion. In the control group, rats underwent a sham operation without agar injection. Injection sites were examined with a light micrograph after compression of the trigeminal ganglion. Air-puff thresholds (mechanical allodynia) were evaluated 3 days before surgery and 3, 7, 10, 14, 17, 21, 24, 30, and 40 days after surgery. Air-puff thresholds significantly decreased after compression of the trigeminal ganglion. Mechanical allodynia was established within 3 days and remained strong over 24 days, returning to preoperative levels approximately 40 days following compression. After subcutaneous injection of 5% formalin ($50{\mu}L$) in the compression of the trigeminal ganglion-treated rats, nociceptive scratching behavior was recorded for 9 successive 5-min internals. Injection of formalin into the vibrissa pad significantly increased the number of scratches and duration of noxious behavioral responses in sham-treated rats. Noxious behavioral responses induced by subcutaneous formalin administration were significantly potentiated in rats with trigeminal ganglion compression. These findings suggest that compression of the trigeminal ganglion enhanced formalin-induced infla-mmatory pain in the orofacial area.

Myositis as an Initial Presentation of Ulcerative Colitis before Gastrointestinal Symptoms

  • Kim, Doo Ri;Kim, DongSub;Choi, SangJoon;Suh, Yeon-Lim;Yoo, So-Young;Kim, Mi Jin;Choe, Yon Ho;Kim, Yae-Jean
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • v.23 no.3
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    • pp.297-303
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    • 2020
  • The musculoskeletal system can be involved as an extra-intestinal manifestation of inflammatory bowel disease. Among these, myositis in ulcerative colitis (UC) is very rare. A 14-year-old girl was admitted due to severe shoulder tenderness. She had complained of left jaw pain and swelling for the past 10 days. Inflammatory markers were elevated with no evidence of infectious etiology. Myositis was suspected by shoulder magnetic resonance imaging. Three days after admission, she developed hematochezia. Muscle biopsy and colonoscopy was performed due to worsening left mandibular area pain and persistent hematochezia. Colonoscopy showed consistent findings with UC. She was finally diagnosed with UC with myositis as an extra-intestinal manifestation. She showed a dramatic response to UC treatment. Gastrointestinal symptoms were well-controlled. After 14 months, UC symptoms and muscle pain were aggravated, which were relieved after steroid and cyclosporin treatment. We report a unique case of UC initially presented with myositis, preceding gastrointestinal symptoms.

Botulinum Toxin Type A Attenuates Activation of Glial Cells in Rat Medullary Dorsal Horn with CFA-induced Inflammatory Pain

  • Kim, Min-Ji;Cho, Jin-Ho;Kim, Hye-Jin;Yang, Kui-Ye;Ju, Jin-Sook;Lee, Min-Kyung;Park, Min-Kyoung;Ahn, Dong-Kuk
    • International Journal of Oral Biology
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    • v.40 no.2
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    • pp.71-77
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    • 2015
  • The activation of glial cells in the spinal cord has been contribute to the initiation and maintenance of pain facilitation induced by peripheral inflammation and nerve injury. The present study investigated effects of botulinum toxin type A (BoNT-A), injected subcutaneously or intracisternally, on the expression of microglia and astrocytes in rats. Complete Freund's Adjuvant (CFA)-induced inflammation was employed as an orofacial chronic inflammatory pain model. A subcutaneous injection of $40{\mu}L$ CFA into the vibrissa pad was performed under 3% isoflurane anesthesia in SD rats. Immunohistochemical analysis for changes in Iba1 (a microglia marker) and GFAP (an astrocyte marker), were performed 5 days after CFA injection. Subcutaneous injection of CFA produced increases in Iba1 and GFAP expression, in the ipsilateral superficial lamia I and II in the medullary dorsal horn of rats. Subcutaneous treatment with BoNT-A attenuated the up-regulation of Iba1 and GFAP expressions induced by CFA injection. Moreover, intracisternal injection of BoNT-A also attenuated the up-regulated Iba1 and GFAP expressions. These results suggest that the anti-nociceptive action of BoNT-A is mediated by modulation activation of glial cells, including microglia and astrocyte.

Influence of pain-relieving therapies on inflammation and the expression of proinflammatory neuropeptides after dental bleaching treatment

  • da Silva, Livia Maria Alves Valentim;Cintra, Luciano Tavares Angelo;de Oliveira Gallinari, Marjorie;Benetti, Francine;Rahal, Vanessa;Ervolino, Edilson;de Alcantara, Sibele;Briso, Andre Luiz Fraga
    • Restorative Dentistry and Endodontics
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    • v.45 no.2
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    • pp.20.1-20.14
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    • 2020
  • Objectives: To minimize the tooth sensitivity caused by in-office bleaching, many dentists use non-steroidal anti-inflammatory drugs and topical desensitizing gels containing potassium nitrate and sodium fluoride. This study aimed to evaluate the influence of these substances on inflammation and the expression of substance P and calcitonin gene-related peptide in pulp nerve fibers. Materials and Methods: Seventy-two rats were divided into 6 groups as follows: GI, control; GII, only dental bleaching; GIII, only ibuprofen; GIV, ibuprofen administered 30 minutes before and after the bleaching treatment and every 12 hours until the analysis; GV, only topical application of a desensitizing agent; and GVI, topical application of a desensitizing agent before dental bleaching. Placebo gel was applied to the upper left jaw and the bleaching agent was applied to the upper right jaw in all groups. Subsequently, the groups were divided into 3 subgroups based on the time of analysis: 0, 24, and 48 hours after bleaching (n = 8). The rats were euthanized and the maxillae were processed and evaluated by histopathological and immunohistochemical analyses. The data were analyzed using the Kruskal-Wallis test, followed by the Dunn test (p < 0.05). Results: In the bleaching groups, the inflammatory process and expression of neuropeptides decreased over time. The animals in which a desensitizing agent was applied showed better results within 24 hours. Conclusions: The use of a desensitizing agent had positive effects on inflammation and pain-related neuropeptide expression, minimizing the painful effects of dental bleaching treatment.

The Role of the Peripheral Chemokine, CCL3, in Hyperalgesia following Peripheral Nerve Injury in the Rat (신경손상에 의해 유발된 과민통반응에서 말초 케모카인 CCL3의 역할)

  • Leem, Joong Woo;Lee, Hyun Joo;Nam, Taick Sang;Yoon, Duck Mi
    • The Korean Journal of Pain
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    • v.21 no.3
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    • pp.187-196
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    • 2008
  • Background: Upregulation of one type of the pro-inflammatory chemokine (CCL2) and its receptor (CCR2) following peripheral nerve injury contributes to the induction of neuropathic pain. Here, we examined whether another type of chemokine (CCL3) is involved in neuropathic pain. Methods: We measured changes in mechanical and thermal sensitivity in the hind paws of naïve rats or rats with an L5 spinal nerve ligation (SNL) after intra-plantar injection of CCL3 or met-RANTES, an antagonist of the CCL3 receptor, CCR1. We also measured CCL3 levels in the sciatic nerve and the hind paw skin as well as CCR1 expression in dorsal root ganglion (DRG) cells from the lumbar spinal segments. Results: Intra-plantar injection of CCL3 into the hind paw of naive rats mimicked L5 SNL-produced hyperalgesia. Intra-plantar injection of met-RANTES into the hind paw of rats with L5 SNL attenuated hyperalgesia. L5 SNL increased CCL3 levels in the sciatic nerve and the hind paw skin on the affected side. The number of CCR1-positive DRG cells in the lumbar segments was not changed following L5 SNL. Conclusions: Partial peripheral nerve injury increases local CCL3 levels along the degenerating axons during Wallerian degeneration. This CCL3 binds to its receptor, CCR1, located on adjacent uninjured afferents, presumably nociceptors, to induce hyperalgesia in the neuropathic pain state.