• 한국임상수의학회지
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• 제17권1호
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• pp.76-82
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• 2000

This study was undertaken to find out the effect of persimmon leaves on histopathological changes of cadmium toxicity in mice. Seventy two BALB/c mice of male were divided into a control group(A) and five experimental groups (B, C, D, E, F) : group A received tap water and basal diet, group B received tap water and diet supplemented with 3% persimmon leaves alone, group C received basal diet and 300 ppm cadmium, group D, E and F received basal diet supplemented with 1, 3% and 7% persimmon leaves and 300 ppm cadmium respectively. Cadmium dissolved in tap water was used, and the persimmon leaves were mixed with feed. All mice were dissected on the 84th day. Pathological changes in liver, kidney, cortical osseous tissue of femoral shaft, bone trabecular of femur, and epiphyseal cartilage plate of femur were observed. Group B showed no significant changes as the control group. But group C showed the unclearness of specific cells in liver, the loss of architecture and necrosis of hepatocyte, degeneration and necrosis of renal convoluted tubules, desquamation and vacuolization of the greater part of the renal tubular epithelium, marked thinning of the cortical osseous tissue in femoral shaft, reduction of cancellous bone volume and decreaswe of trabecular number, and marked thinning of epiphyseal cartilage plate in femur. On the other hand, persimmon leaves-treated group showed a little convalescent changes an maintained their normal architectures in liver, kidney, cortical osseous tissue of femoral shaft, bone trabecular of femur, and epiphyseal cartilage plate of femur.

• 한국식품영양과학회지
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• 제26권3호
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• pp.475-479
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• 1997

A decrease in the circulating levels of estrogen, occuring as a consequence of post menopausal decline or from surgical ovariectomy, results in an accelerated loss of bone. Estrogen has been shown to stimulate lysyl oxidase activity, and the treatment with estrogen increased the pyridinium content of cortical bone. a trivalent mature cross-links collagen fibrils named pyridinoline, which is especially abundant in collagen of cartilage and bone, markedly increases with growth in humans and rats. The main aim of this study was to examine the increased bone loss caused by ovariectomy through monitoring the concentrations of the collagen and the pyridinium cross-links of collagen, pyridinoline. The ovariectomized rats, 4 weeks old, were divided at random into two or three groups of 5. Ovariectomies were carried out on both of the saline-treated group(OVX(NH)) and the estrogen-treated group(OVX(H)) using the dorsal approach and sham operations were performed on the sham-operated group(sham). They were maintained under identical conditions for 4 or 8 weeks and were allowed free access to food and water. it was observed that there was no significant difference between the control group and the sham-operated group, however, the control group had a higher content of collagen than the saline-treated group after 4 weeks and 8 weeks. Based on these results, iot is supposed that estrogen can enhance collagen synthesis and affects the pyridinoline formation in collagen fibrils through stimulating lysyl oxidase activity.

• IMMUNE NETWORK
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• 제14권1호
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• pp.45-53
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• 2014

Osteoarthritis (OA) is a degenerative joint disease characterized by a progressive loss of cartilage. And, increased oxidative stress plays a relevant role in the pathogenesis of OA. Ursodeoxycholic acid (UDCA) is a used drug for liver diseases known for its free radical-scavenging property. The objectives of this study were to investigate the in vivo effects of UDCA on pain severity and cartilage degeneration using an experimental OA model and to explore its mode of actions. OA was induced in rats by intra-articular injection of monosodium iodoacetate (MIA) to the knee. Oral administration UDCA was initiated on the day of MIA injection. Limb nociception was assessed by measuring the paw withdrawal latency and threshold. Samples were analyzed macroscopically and histologically. Immunohistochemistry was used to investigate the expression of interleukin-$1{\beta}$ (IL-$1{\beta}$), IL-6, nitrotyrosine and inducible nitric oxide synthase (iNOS) in knee joints. UDCA showed an antinociceptive property and attenuated cartilage degeneration. OA rats given oral UDCA significantly exhibited a decreased number of osteoclasts in subchondral bone legion compared with the vehicle-treated OA group. UDCA reduced the expression of IL-$1{\beta}$, IL-6, nitrotyrosine and iNOS in articular cartilage. UDCA treatment significantly attenuated the mRNA expression of matrix metalloproteinase-3 (MMP-3), -13, and ADAMTS5 in IL-$1{\beta}$-stimulated human OA chondrocytes. These results show the inhibitory effects of UDCA on pain production and cartilage degeneration in experimentally induced OA. The chondroprotective properties of UDCA were achieved by suppressing oxidative damage and inhibiting catabolic factors that are implicated in the pathogenesis of cartilage damage in OA.

• 대한기관식도과학회지
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• 제8권1호
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• pp.75-80
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• 2002

Radiation therapy is an effective treatment modality for malignant disease of the head and neck, but it is not without risk and complication. Response of the larynx to radiotherapy varies from mild erythema to severe inflammation with edema and induration. possibly leading to necrosis of cartilage. These changes are due to an inflammatory reaction characterized by infiltration of polymorphonuclear leukocytes, vascular thrombosis, and obliteration of lymphatic channels. Late changes consist of telangiectasia of the skin, alopecia, loss of subcutaneous fat, degenerative changes in the connective tissues. But, radiation necrosis of laryngeal cartilage is an uncommon complication and it is a devastating process for which further necessitates surgical treatment. It is generally agreed that the only treatment for patient not responding to conservative measures is a total laryngectomy. We experienced 4 cases of delayed radionecrosis of the larynx who underwent radiation therapy for glottic cancer and hypopharyngeal cancer. We report these cases with review of literature.

• 한국임상수의학회지
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• 제18권2호
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• pp.116-123
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• 2001

This study was undertaken to find out the effect of Korean safflower seed powder on histopathological changes of cadmium toxicity in mice. Fifty BALB/c mice were divided into a control group(A) and four experimental groups(B, C, D, E) : group A received tap water and basal diet, group B received tap water and diet supplemented with 3% Korean safflower seed powder alone, group C received basal diet and 300 $\mu\textrm{g}$/g of cadmium, group D and E received basal diet supplemented with 3% and 10% Korean safflower seed powder and 300$\mu\textrm{g}$/g of cadmium respectively. Cadmium dissolved in tap water was used, and the Korean safflower seed powder were mixed with feed. All mice were dissected on the 56th day. Histopathological changes in liver, kidney, lung, cortical osseous tissue of femoral shaft, bone trabecular of femur, and epiphyseal cartilage plate of femur were observed. Group B showed no significant changes compared with the control group. But group C showed the unclearness of specific cells in liver, the loss of architecture and focal necrosis of hepatocyte, the glomerular swelling, degeneration and necrosis of convoluted tubules, desquamation and vacuolization of the greater part of the renal tubular epithelium, the marked congestion and thickness of the wall of alveolus in lung, slightly thinning of the cortical osseous tissue in femoral shaft, reduction of cancellous bone volume and marked narrowness of bone trabecular, marked thinning of epiphyseal cartilage plate and irregular arrangement of columnar structure of cartilage cells. On the other hand, Korean safflower seed powder-treated group showed a little convalescent changes and maintained their normal architectures in liner, kidney, lung, cortical osseous tissue of femoral shaft, bone trabecular of femur and epiphyseal cartilage plate of femur.

• The Journal of Korean Physical Therapy
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• 제26권6호
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• pp.418-424
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• 2014

Purpose: This study was performed to investigate the effect of joint mobilization on pain relief and cartilage repair in an induced osteoarthritis rat model by analyzing the expression of heat shock protein 70 in articular cartilage. Methods: MIA was injected into SD rats to induce osteoarthritis. These rats were divided into 4 groups: control group (n=30), no further treatment after the MIA injection ; experimental group I(n=30), performed swimming exercise after the MIA injection experimental group II (n=30), underwent joint mobilization after the MIA injection and experimental group III (n=30), performed swimming exercise and underwent joint mobilization after the MIA injection. For the histologic and pathophysiologic evaluation, safranin-O staining and for the immunohistochemical evaluation, the expression of HSP 70 in articular cartilage was analyzed 1, 7, 14, and 21 days after the MIA injection. Results: The inflammatory response and loss of tissue declined in experimental groups I and II over time, whereas the greatest decreases were noted in experimental group III. In the articular cartilage, low expression of HSP 70 was observed in every group on day 1, whereas HSP 70 expression was elevated on days 7 and 14 in experimental groups II and III. After 21 days, experimental group II displayed the strongest positive reaction, whereas HSP 70 was higher in experimental group III at this time point compared to that after 14 days. Conclusion: Our results showed that swimming exercise and joint mobilization had positive effects on pain relief and histologic and functional recovery in an induced osteoarthritis rat model.

• Journal of Microbiology and Biotechnology
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• 제31권10호
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• pp.1401-1408
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• 2021

This study examined whether the oral administration of low-molecular-weight collagen peptide (LMCP) containing 3% Gly-Pro-Hyp with >15% tripeptide (Gly-X-Y) content could ameliorate osteoarthritis (OA) progression using a rabbit anterior cruciate ligament transection (ACLT) model of induced OA and chondrocytes isolated from a patient with OA. Oral LMCP administration (100 or 200 mg/kg/day) for 12 weeks ameliorated cartilage damage and reduced the loss of proteoglycan compared to the findings in the ACLT control group, resulting in dose-dependent (p < 0.05) improvements of the OARSI score in hematoxylin & eosin (H&E) and Safranin O staining. In micro-computed tomography analysis, LMCP also significantly (p < 0.05) suppressed the deterioration of the microstructure in tibial subchondral bone during OA progression. The elevation of IL-1β and IL-6 concentrations in synovial fluid following OA induction was dose-dependently (p < 0.05) reduced by LMCP treatment. Furthermore, immunohistochemistry illustrated that LMCP significantly (p < 0.05) upregulated type II collagen and downregulated matrix metalloproteinase-13 in cartilage tissue. Consistent with the in vivo results, LMCP significantly (p < 0.05) increased the mRNA expression of COL2A1 and ACAN in chondrocytes isolated from a patient with OA regardless of the conditions for IL-1β induction. These findings suggest that LMCP has potential as a therapeutic treatment for OA that stimulates cartilage regeneration.

• 대한치과교정학회지
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• 제24권3호
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• pp.569-586
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• 1994

성장기 백서에 있어서 상악 및 하악 절치의 제거와 soft diet 투여시에 있어서 하악과두의 후상부와 상부에서의 연골의 성장, 연골층의 두께 및 미세구조 그리고 교근의 천층 및 악이복근의 근섬유에 미치는 영향을 요약하면 다음과 같다. 과두연골의 후상부 및 상부에서, 섬유층과 증식층의 두께가 대조군에 비해 유의하게 감소하였으며(p<0.01), 후상부에서의 감소정도는 상부보다 컸었다. 그러나 성숙세포층, 비대세포층 및 연골 전체의 두께는 대조군에 비해 차이가 없었다. $^3H-thymidine$투여 후 시간경과에 따른 각 층의 세포표지율은 상부에서는 대조군에 비해 차이가 없었으나 후상부에서는 투여후 1일과 2일 경과군에서는 성숙세포층, 4일 경과군에서는 비대세포층의 표지율이 대조군에 비해 유의하게 감소하므로서 (p<0.01) 상악 및 하악 절치의 제거와 soft diet투여로 과두 후상부에 가해지는 기계적 부하의 감소로 인해 이 부위의 연골성장이 감소되는 것으로 나타났다. 대조군에 있어서, 하악과두는 상부에 비해 후 상부방향으로 더 빨리 성장하는 것으로 나타났다. 교근의 천층에서, type IIA 근섬유의 직경은 변화하지 않았으나 type IIB 근섬유의 직경은 대조군에 비해 유의하게 감소하였다 (P<0.01). 악이복근의 전복에서, type I 근섬유의 직경은 변화하지 않았으나 type IIA, type IIB 근섬유의 직경은 대조군에 비해 유의하게 감소하였다(P<0.01). 하악과두 연골의 미세구조에 있어서는 증식층, 성숙세포층 및 비대세포층은 모두 후상부와 상부에서 대조군에 비해 유의할 만한 변화가 없었다. 그러나 섬유층에서, 상부에서는 대조군에 비해 차이가 없었으나 후상부에서는 뚜렷한 차이가 있었다. 실험군 후상부의 섬유층에서는 대조군처럼 관절강에 인접한 세포와 증식층에 인접한 세포사이의 미세구조적 차이는 인지되지 않았으며, 흡수기능을 가진 세포에서 보이는 손가락 모양의 많은 세포돌기, 세포막을 따라 나타나는 수 많은 미음소포, 발달된 용해소체, 사립체 그리고 불규칙한 모양의 핵 등과 같은 대조군의 관절강에 인접한 세포에서 많이 나타나는 특징은 미약하였으며 전반적으로 세포간 기질을 개조하는 활동이 감소하는 양상을 보였다.

• BMB Reports
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• 제54권10호
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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.

• IMMUNE NETWORK
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• 제22권2호
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• pp.14.1-14.17
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• 2022

Osteoarthritis (OA) is a common degenerative joint disease characterized by breakdown of joint cartilage. Mitochondrial dysfunction of the chondrocyte is a risk factor for OA progression. We examined the therapeutic potential of mitochondrial transplantation for OA. Mitochondria were injected into the knee joint of monosodium iodoacetate-induced OA rats. Chondrocytes from OA rats or patients with OA were cultured to examine mitochondrial function in cellular pathophysiology. Pain, cartilage destruction, and bone loss were improved in mitochondrial transplanted-OA rats. The transcript levels of IL-1β, TNF-α, matrix metallopeptidase 13, and MCP-1 in cartilage were markedly decreased by mitochondrial transplantation. Mitochondrial function, as indicated by membrane potential and oxygen consumption rate, in chondrocytes from OA rats was improved by mitochondrial transplantation. Likewise, the mitochondrial function of chondrocytes from OA patients was improved by coculture with mitochondria. Furthermore, inflammatory cell death was significantly decreased by coculture with mitochondria. Mitochondrial transplantation ameliorated OA progression, which is caused by mitochondrial dysfunction. These results suggest the therapeutic potential of mitochondrial transplantation for OA.