• Korean Journal of Pharmacognosy
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• v.37 no.3
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• pp.136-142
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• 2006

New herbal formula (NHF) is the ethanol extract mixture of Puerariae radix, Artemisia capillaries and Perilla frutescens. We have Investigated the effects on anti-inflammation by NHF and attempted acetic acid induced writhing to verify the analgesic effect. Macrophages and chondrocytes were obtained from mouse and rabbit. Inflammation was induced bγ interleukin-1, tumor necrosis $factor-{\alpha}$, $interferon-{\gamma}$, and lipopolysaccharide. NHF showed strong inhibitory efficacy against cytokine-induced proteoglycan degradation, $PGE_2$ production, NO production, and MMP-9 expression in rabbit articular chondrocyte. In the writhing test, NHF exhibited a dose-dependent inhibition of writhing. Futhermore, NHF increased the activity of SOD. NHF have anti-inflammatory and analgesic activities, and could be a good herbal medicine candidate for curing of osteoarthritis.

• Korean Journal of Pharmacognosy
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• v.36 no.4 s.143
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• pp.338-343
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• 2005

Inflammatory mediators such as interleukin-1 (IL-1), tumor necrosis $factor-{\alpha}\;(TNF-{\alpha}),\;interferon-{\gamma}\;(IFN-{\gamma})$ and lipopolysaccharide (LPS) are thought to play major roles in joint diseases such as a rheumatoid arthritis (RA), and there is considerable evidence playing a role for these cytokines in osteoarthritis (OA). Therefore, we have studied the effects on anti-inflammation and analgesic by ethyl acetate fraction from 70% ethanol extract of Artemisia capillaries (EAC). As a positive control, apigenin, which is known as an anti-inflammatory agent as an iNOS inhibitor, was used and showed the dose-dependent inhibitory effect. EAC showed strong inhibitory efficacy against cytokine-induced proteoglycan degradation, $PGE_2$ production, nitric oxide (NO) production, and matrix-matalloproteinases (MMPs) expression in rabbit articular chondrocyte. In the writhing test induced by acetic acid, EAC $(200{\sim}400\;mg/kg)$ exhibited a dose-dependent inhibition of writhing. The results indicate that EAC have anti-inflammatory and analgesic activities, and could be a good herbal medicine candidate for curing of RA and/or OA.

• Journal of Marine Bioscience and Biotechnology
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• v.12 no.2
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• pp.99-107
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• 2020

Osteoarthritis (OA) is an inflammatory degenerative joint disease that is accompanied by irreversible joint cartilage destruction. Recently, the antioxidant effects of Carpomitra costata, which is a type of brown algae, have been reported, but their effects on OA have not been investigated. In this study, the anti-osteoarthritic effect of the ethanol extract of C. costata (EECC) on SW1353 human chondrocytes was studied. Results showed that EECC significantly attenuated the interleukin-1β (IL-1β)-induced release of pro-inflammatory mediators, including prostaglandin E2 and nitric oxide (NO), as well as expressions of cyclo-oxygenase-2 and inducible NO synthase. EECC also inhibited the IL-1β-induced expressions of matrix metalloproteinase-1, -3, and -13 in SW1353 chondrocytes, which reduced their extracellular secretion. In addition, the oxidative stress induced by IL-1β was confirmed to be blocked by EECC due to the inhibition of reactive oxygen species generation. Moreover, EECC suppressed IL-1β-mediated translocation of nuclear factor-kappa B (NF-κB) from cytosol into the nucleus and the degradation of IκB-α, which indicates that EECC exhibits anti-inflammatory effects by inhibiting the NF-κB signaling pathway. These results are the first to demonstrate the anti-inflammatory activities of C. costata extracts in chondrocytes, thus suggesting that this algae extract may be used in the treatment of OA.

• Journal of Veterinary Clinics
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• v.37 no.5
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• pp.261-269
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• 2020

The purpose of this study is to investigate the clinical effects of carboxymethyl chitosan (CMC) and adipose-derived mesenchymal stem cells (MSCs) on osteoarthritis (OA). Thirty New Zealand white rabbits were used as cranial cruciate ligament transection and partial meniscectomy models. The rabbits were divided into five groups (n = 6) according to the intra-articular injection materials: the control group with PBS, the HA group with hyaluronic acid, the CMC group with CMC, the MSC group with MSCs emerged in PBS, and the MSC+CMC group with CMC and MSCs. Knee thickness, extension angle, gross morphology, histopathology and immunohistochemistry were performed to evaluate the effects of CMC and MSCs on rabbit OA. On the morphologic and histologic examination, the articular surfaces of the femur and tibia were markedly damaged in control group with higher Mankin score and lower cartilage surface thickness. However, OA related cartilage defects were alleviated by the treatment of MSC and/or CMC. The expressions of apoptotic and inflammatory cytokines were decreased and cartilage extracellular matrix (ECM) related collagens I and II were enhanced by the treatment of MSC and/or CMC. In conclusion, this study showed that CMC and MSC treatments have a beneficial effects on OA via the protection of cartilage damage, the stimulation of ECM, and the inhibition of inflammatory and apoptotic reaction.

• Korean Journal of Medicinal Crop Science
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• v.21 no.6
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• pp.466-473
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• 2013

This study investigates the effect of supercritical fluid extract (CMPB803-C) of Lithospermum erythrorhizon, shikonin and acetylshikonin isolated from Lithospermum erythrorhizon on IL-$1{\beta}$-induced chondrocytes and monosodium iodoacetate (MIA)-induced osteoarthritis in rat. Shikonin ($50{\mu}m$) and acetylshikonin ($3{\mu}M$) treatment reduced significantly the mRNA expression and enzyme activity of matrix metalloproteinase (MMP)-1, -3 and -13 in IL-$1{\beta}$-induced SW1353 chondrosarcoma cells. The chondro-protective effects of CMPB803-C and acetylshikonin were than analyzed in a rat OA model using a single intra-articular injection of MIA (1mg) in the right knee joint. CMPB803-C (200mg/kg) or acetylshikonin (5mg/kg) was orally administered daily for two weeks starting after 1 week of MIA injection. In the histological observation, CMPB803-C and acetylshikonin clearly improved OA lesions being comparable to or better that control group. Our results demonstrated that CMPB803-C and acetylshikonin as active compound of Lithospermum erythrorhizon have a strong chondro-protective effect in OA rats, which likely attributes to its anti-inflammatory activity and inhibition of MMPs production.

• Journal of the Korean Society of Physical Medicine
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• v.8 no.4
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• pp.539-547
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• 2013

PURPOSE: This study examined the effects of exercise of diverse intensities on the expression of TNF-${\alpha}$(tumor necrosis factor-${\alpha}$) in the spinal cord in osteoarthritic rats. METHODS: Over a period of four weeks, the authors applied treadmill exercise programs of diverse intensities to Sprague-Dawley rats, to which intra-articular injection of monosodium iodoacetate(MIA, $3mg/50{\mu}l$, diluted in saline) was applied to the right knee joint to induce osteoarthritis. The four-week exercise program was not carried out with the control group(CG, n=10). Exercise programs of applicable intensities were applied to the low-intensity exercise group(LEG, n=10), moderate-intensity exercise group (MEG, n=10), and high-intensity exercise group(HEG, n=10) over the four weeks. Observations were made of expression of TNF-${\alpha}$ in the spinal cord in osteoarthritic rats using western blot analysis. RESULT: there were significant differences(p<.05) in the comparison of expression of TNF-${\alpha}$ between the four groups involved. The expression of TNF-${\alpha}$ in the spinal cord, the LEG and HEG had more elevated expression significantly than the CG(p<.05). But the MEG had reduced expression significantly than the CG(p<.05). CONCLUSION: These study results suggest that moderate-intensity exercise is effective in inhibition TNF-${\alpha}$ in the spinal cord. They also indicate that in prescribing exercise to treat osteoarthritic patients, exercise of moderate intensity is most suitable to patients' chronic pain, rather than low or high intensity.

• BMB Reports
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• v.54 no.10
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• pp.528-533
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• 2021

Osteoarthritis (OA) is a degenerative disorder that can result in the loss of articular cartilage. No effective treatment against OA is currently available. Thus, interest in natural health products to relieve OA symptoms is increasing. However, their qualities such as efficacy, toxicity, and mechanism are poorly understood. In this study, we determined the efficacy of avenanthramide (Avn)-C extracted from oats as a promising candidate to prevent OA progression and its mechanism of action to prevent the expression of matrix-metalloproteinases (MMPs) in OA pathogenesis. Interleukin-1 beta (IL-1β), a proinflammatory cytokine as a main causing factor of cartilage destruction, was used to induce OA-like condition of chondrocytes in vitro. Avn-C restrained IL-1β-mediated expression and activity of MMPs, such as MMP-3, -12, and -13 in mouse articular chondrocytes. Moreover, Avn-C alleviated cartilage destruction in experimental OA mouse model induced by destabilization of the medial meniscus (DMM) surgery. However, Avn-C did not affect the expression of inflammatory mediators (Ptgs2 and Nos) or anabolic factors (Col2a1, Aggrecan, and Sox9), although expression levels of these genes were upregulated or downregulated by IL-1β, respectively. The inhibition of MMP expression by Avn-C in articular chondrocytes was mediated by p38 kinase and c-Jun N-terminal kinase (JNK) signaling, but not by ERK or NF-κB. Interestingly, Avn-C added with SB203580 and SP600125 as specific inhibitors of p38 kinase and JNK, respectively, enhanced its inhibitory effect on the expression of MMPs in IL-1β treated chondrocytes. Taken together, these results suggest that Avn-C is an effective candidate to prevent OA progression and a natural health product to relieve OA pathogenesis.

• Korean Journal of Pharmacognosy
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• v.49 no.4
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• pp.305-311
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• 2018

Osteoarthritis (OA) is the most common form of joint disease, characterized by articular cartilage, osteonecrosis, and osteochondral bone erosion. It is an early, progressive disease that combines joint stiffness and joint pain and reduces cartilage function and condition. Interleukin-1 beta ($IL-1{\beta}$) is thought to be important to the pathogenesis of OA and significantly increases the expression of matrix metalloproteinases (MMPs), which play an important role in cartilage degradation in OA. Sparassis crispa (Wulf.) is an edible / medicinal mushroom that has been reported to variety of biological activities. In this study, investigated the Anti-inflammatory effect of Sparassis crispa (Wulf.) ethanol extract (SCE) on $IL-1{\beta}$ stimulated SW1353 chondrocytes. SCE decreased the expression and activity of MMPs by $IL-1{\beta}$ and decreased the levels of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) associated with the inhibition of prostaglandin E2($PGE_2$) in $IL-1{\beta}$ stimulated SW-1353 chondrocytes. In addition, SCE inhibits the expression of MAPK (mitogen-activated protein kinase) and $NF-{\kappa}B$ (nuclear factor-kappa B) signaling in $IL-1{\beta}$ stimulated SW-1353 cells, and SCE inhibits the production of reactive oxygen species (ROS) through heme oxygenase-1 (HO-1) expression. Thus, it is suggested that SCE has a potential as an anti-inflammatory agent in osteoarthritis treatments.

• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.1
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• pp.28-34
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• 2006

The ethanol extracts of Puerariae Radix inhibited cyclooxygenase-2 (COX-2) activity in bone marrow derived mast cells (BMMC). COX-2 is responsible for the production of large amounts of proinflammatory prostaglandins (PGs) at the inflammatory site. We have investigated the anti-inflammatory effect of ethyl acetate fraction from $70\%$ ethanol extract of Puerariae Radix (EPR), and attempted acetic acid induced writhing to verify the analgesic effect. Inflammation was induced by interleukin-1 (IL-1), tumor necrosis factor-a (TNF-a), $inteferon-\gamma$ $(IFN-\gamma)$ and lipopolysaccharide (LPS). EPR showed strong inhibitory efficacy against cytokine-induced proteoglycan degradation, prostaglandin $E_2\;(PGE_2)$ production, nitric oxide (NO) production, and matrix-metalloproteinases (MMPs) expression in mouse macrophage and rabbit articular chondrocyte. In the writhing test, EPR $(200\~400\;mg/kg)$ exhibited a dose-dependent inhibition of writhing. The results indicate that EPR have anti-inflammatory and analgesic activities, and could be a good herbal medicine candidate for treating of osteoarthritis (OA).

• Analytical Science and Technology
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• v.28 no.6
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• pp.361-369
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• 2015

The precise mechanism underlying the therapeutic efficacy of an extraction powder of Angelica gigas (AGE) for the treatment of degenerative osteoarthritis was investigated in primary cultured rabbit chondrocytes and in a monosodium-iodoacetate (MIA)-induced osteoarthritis rat model. The treatment with AGE (50 μg/mL) effectively inhibited NF-B activation. The anti-inflammatory mechanism was clarified by gelatin zymography and western blotting measurements of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) activities. The AGE (50 μg/mL) treatment significantly reduced MMP-9 activity. The constituents of AGE— decursinol, decursin, and decursinol angelate—were determined by LC-MS/MS after a 24 hr treatment of rabbit chondrocytes. The contents of the major products, decursin and decursinol angelate, were 3.62±0.47 and 2.14 ±0.36 μg/mg protein, respectively in AGE-treated (50 μg/mL) rabbit chondrocytes. An in vivo animal study on rats fed a diet containing 25, 50, and 100 mg/kg AGE for 3 weeks revealed a significant inhibition of the MMPs in the MIA-induced rat articular cartilage. The genetic expression of arthritic factors in the articular cartilage was examined by RT-PCR of collagen Type I, collagen Type II, aggrecan, and MMP (MMP3, MMP-9, MMP13). Specifically, AGE up-regulated the expression of collagen Type I, collagen Type II, and aggrecan and inhibited MMP levels at all tested concentrations. Collectively, AGE showed a strong specific site of action on MMP regulation and protected against the degeneration of articular cartilage via cellular regulation of MMP expression both in vitro and in vivo.