scholarly journals Intra-Articular Injection of Fructus Ligustri Lucidi Extract Attenuates Pain Behavior and Cartilage Degeneration in Mono-Iodoacetate Induced Osteoarthritic Rats

2018 ◽  
Vol 9 ◽  
Author(s):  
Bo Yan ◽  
Li Zhou ◽  
Caiwei Wang ◽  
Rongrong Wang ◽  
Li Yan ◽  
...  
Keyword(s):  
Cartilage Degeneration ◽  
Pain Behavior ◽  
Fructus Ligustri Lucidi ◽  
And Cartilage

scholarly journals Exosomes derived from miR-126-3p-overexpressing synovial fibroblasts suppress chondrocyte inflammation and cartilage degradation in a rat model of osteoarthritis

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yan Zhou ◽  
Jianghua Ming ◽  
Yaming Li ◽  
Bochun Li ◽  
Ming Deng ◽  
...  
Keyword(s):  
Synovial Fluid ◽  
Apoptotic Cell ◽  
Synovial Fibroblasts ◽  
Cartilage Degeneration ◽  
Cartilage Degradation ◽  
Exosomal Mirnas ◽  
Exosomal Mirna ◽  
And Control ◽  
And Cartilage

AbstractMicroRNAs (miRNAs) encapsulated within exosomes can serve as essential regulators of intercellular communication and represent promising biomarkers of several aging-associated disorders. However, the relationship between exosomal miRNAs and osteoarthritis (OA)-related chondrocytes and synovial fibroblasts (SFCs) remain to be clarified. Herein, we profiled synovial fluid-derived exosomal miRNAs and explored the effects of exosomal miRNAs derived from SFCs on chondrocyte inflammation, proliferation, and survival, and further assessed their impact on cartilage degeneration in a surgically-induced rat OA model. We identified 19 miRNAs within synovial fluid-derived exosomes that were differentially expressed when comparing OA and control patients. We then employed a microarray-based approach to confirm that exosomal miRNA-126-3p expression was significantly reduced in OA patient-derived synovial fluid exosomes. At a functional level, miRNA-126-3p mimic treatment was sufficient to promote rat chondrocyte migration and proliferation while also suppressing apoptosis and IL-1β, IL-6, and TNF-α expression. SFC-miRNA-126-3p-Exos were able to suppress apoptotic cell death and associated inflammation in chondrocytes. Our in vivo results revealed that rat SFC-derived exosomal miRNA-126-3p was sufficient to suppress the formation of osteophytes, prevent cartilage degeneration, and exert anti-apoptotic and anti-inflammatory effects on articular cartilage. Overall, our findings indicate that SFC exosome‐delivered miRNA-126-3p can constrain chondrocyte inflammation and cartilage degeneration. As such, SFC-miRNA-126-3p-Exos may be of therapeutic value for the treatment of patients suffering from OA.

scholarly journals Early patellofemoral articular cartilage degeneration in a rat model of patellar instability is associated with activation of the NF-κB signaling pathway

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Wei Lin ◽  
Huijun Kang ◽  
Yike Dai ◽  
Yingzhen Niu ◽  
Guangmin Yang ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Signaling Pathway ◽  
Subchondral Bone ◽  
Patellofemoral Joint ◽  
Patellar Instability ◽  
Cartilage Degeneration ◽  
Control Group ◽  
And Control ◽  
Articular Cartilage Degeneration ◽  
And Cartilage

Abstract Background Patellar instability (PI) often increases the possibility of lateral patellar dislocation and early osteoarthritis. The molecular mechanism of early articular cartilage degeneration during patellofemoral osteoarthritis (PFOA) still requires further investigation. However, it is known that the NF-κB signaling pathway plays an important role in articular cartilage degeneration. The aim of this study was to investigate the relationship between the NF-κB signaling pathway and patellofemoral joint cartilage degeneration. Methods We established a rat model of PI-induced PFOA. Female 4-week-old Sprague-Dawley rats (n = 120) were randomly divided into two groups: the PI (n = 60) and control group (n = 60). The distal femurs of the PI and control group were isolated and compared 4, 8, and 12 weeks after surgery. The morphological structure of the trochlear cartilage and subchondral bone were evaluated by micro-computed tomography and histology. The expression of NF-κB, matrix metalloproteinase (MMP)-13, collagen X, and TNF-ɑ were evaluated by immunohistochemistry and quantitative polymerase chain reaction. Results In the PI group, subchondral bone loss and cartilage degeneration were found 4 weeks after surgery. Compared with the control group, the protein and mRNA expression of NF-κB and TNF-ɑ were significantly increased 4, 8, and 12 weeks after surgery in the PI group. In addition, the markers of cartilage degeneration MMP-13 and collagen X were more highly expressed in the PI group compared with the control group at different time points after surgery. Conclusions This study has demonstrated that early patellofemoral joint cartilage degeneration can be caused by PI in growing rats, accompanied by significant subchondral bone loss and cartilage degeneration. In addition, the degeneration of articular cartilage may be associated with the activation of the NF-κB signaling pathway and can deteriorate with time as a result of PI.

scholarly journals LOX-1 deficient mice show resistance to zymosan-induced arthritis

2018 ◽  
Author(s):  
Kazuhiko Hashimoto ◽  
Yutaka Oda ◽  
Koichi Nakagawa ◽  
Terumasa Ikeda ◽  
Kazuhiro Ohtani ◽  
...  
Keyword(s):  
Inflammatory Cell ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Cartilage Degeneration ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Synovial Cells ◽  
Synovial Hyperplasia ◽  
And Cartilage

Recent data suggest that the lectin-like oxidized low-density lipoprotein (ox-LDL) receptor-1 (LOX-1)/ox-LDL system may be involved in the pathogenesis of arthritis. We aimed to demonstrate the roles of the LOX-1/ox-LDL system in arthritis development by using LOX-1 knockout (KO) mice. Arthritis was induced in the right knees of C57Bl/6 wild-type (WT) and LOX-1 KO mice via zymosan injection. Saline was injected in the left knees. Arthritis development was evaluated using inflammatory cell infiltration, synovial hyperplasia, and cartilage degeneration scores at 1, 3, and 7 days after administration. LOX-1, ox-LDL, and matrix metalloproteinase-3 (MMP-3) expression in the synovial cells and chondrocytes was evaluated by immunohistochemistry. The LOX-1, ox-LDL, and MMP-3 expression levels in synovial cells were scored on a grading scale. The positive cell rate of LOX-1, ox-LDL, and MMP-3 in chondrocytes was measured. The correlation between the positive cell rate of LOX-1 or ox-LDL and the cartilage degeneration score was also examined. Inflammatory cell infiltration, synovial hyperplasia, and cartilage degeneration were significantly reduced in the LOX-1 KOmice with zymosan-induced arthritis (ZIA) compared to WT mice with ZIA. In the saline-injected knees, no apparent arthritic changes were observed. LOX-1 and ox-LDL expression in synovial cells and chondrocytes were detected in the knees of WT mice with ZIA. No LOX-1 and ox-LDL expression was detected in the knees of LOX-1 KOmice with ZIA or the saline-injected knees of both mice. MMP-3 expression in the synovial cells and chondrocytes was also detected in knees of both mice with ZIA, and was significantly less in the LOX-1 KO mice than in WT mice. The positive cell rate of LOX-1 or ox-LDL and the cartilage degeneration score showed a positive correlation. Our data show the involvement of the LOX-1/ox-LDL system in murine ZIA development. LOX-1-positive synovial cells and chondrocytes are potential therapeutic targets for arthritis prevention.

Relationship Between Bone Marrow Lesions on MRI and Cartilage Degeneration in Osteochondral Lesions of the Talar Dome

2018 ◽  
Vol 39 (8) ◽  
pp. 908-915 ◽  
Author(s):  
Tomoyuki Nakasa ◽  
Yasunari Ikuta ◽  
Mikiya Sawa ◽  
Masahiro Yoshikawa ◽  
Yusuke Tsuyuguchi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Subchondral Bone ◽  
Cartilage Degeneration ◽  
Osteochondral Lesions ◽  
Talar Dome ◽  
Mankin Score ◽  
Osteochondral Fragment ◽  
The Mean ◽  
And Cartilage ◽  
Ct And Mri

Background: In the evaluation of osteochondral lesions of the talar dome (OLT), bone marrow lesions (BML) are commonly observed in the subchondral bone on magnetic resonance imaging (MRI). However, the significance of BML, such as the histology of the overlying cartilage, is still unclear. The purpose of this study was to investigate the relationship between the BML and cartilage degeneration in OLT. Methods: Thirty-three ankles with OLT were included in this study. All ankles underwent CT and MRI and had operative treatment. The ankles were divided into 2 groups, depending on the presence of bone sclerosis (ie, with or without) in the host bone just below the osteochondral fragment (nonsclerosis group and sclerosis group). The area of BML was compared between the 2 groups. Biopsies of the osteochondral fragment from 20 ankles were performed during surgery, and the correlation between the BML and cartilage degeneration was analyzed. The remaining 13 ankles had the CT and MRI compared with the arthroscopic findings. Results: The mean area of BML in the nonsclerosis group was significantly larger than that in the sclerosis group. In the histologic analysis, there was a significant and moderate correlation between the Mankin score and the area of BML. The mean Mankin score in the nonsclerosis group was significantly lower than that in the sclerosis group. Conclusions: This study revealed that a large area of BML on MRI exhibited low degeneration of cartilage of the osteochondral fragment, while a small area of BML indicated sclerosis of the subchondral bone with severe degeneration of cartilage. The evaluation of BML may predict the cartilage condition of the osteochondral fragment. Level of Evidence: Level III, comparative series.

Spontaneous development of synovitis and cartilage degeneration in transgenic mice overexpressing cathepsin K

2005 ◽  
Vol 52 (12) ◽  
pp. 3713-3717 ◽  
Author(s):  
Jukka Morko ◽  
Riku Kiviranta ◽  
Kirsi Joronen ◽  
Anna-Marja Säämänen ◽  
Eero Vuorio ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cathepsin K ◽  
Cartilage Degeneration ◽  
And Cartilage

Dexamethasone induces apoptosis in proliferative canine tendon cells and chondrocytes

2008 ◽  
Vol 21 (04) ◽  
pp. 337-342 ◽  
Author(s):  
M. A. Hossain ◽  
J. Park ◽  
S. H. Choi ◽  
G. Kim
Keyword(s):  
Cell Proliferation ◽  
Cartilage Degeneration ◽  
Dependent Manner ◽  
Tendon Cells ◽  
Cartilage Cells ◽  
In Vitro Effects ◽  
Nuclear Apoptosis ◽  
And Cartilage

SummaryDexamethasone (Dexa) has been commonly used in humans and domestic animals, particularly in the treatment of tendon injuries and cartilage degeneration. However, it is often associated with tendon rupture and impaired tendon and cartilage healing. In the present study, we investigated Dexa’s in vitro effects on the growth of cell proliferation and the induction of apoptosis in canine Achilles tendon cells and chondrocytes. Cell proliferation after treatment with Dexa for two to six days was quantified by a 2,3-bis{2-methoxy- 4-nitro-5-sulfophenyl}-2H-tetrazolium-5-carboxyanilide inner salt assay (XTT). The results showed that Dexa could inhibit the proliferation of tendon cells and chondrocytes at increasing concentrations (0.1–50 μg/ml) compared with untreated cells. Cell apoptosis was induced by Dexa, as evidenced by the typical nuclear apoptosis using Hoechst 33258 staining. Dexa increased the apoptosis of canine tendon cells and chondrocytes in a time-dependent manner. In canine tendon cells and chondrocytes that were treated with 25 and 50 μg/ml concentration of Dexa, the number of condensed apoptotic nuclei was significantly increased. In addition, culturing with Dexa and the glucocorticoid receptor blocker, mifepristone, significantly arrested apoptosis of tendon cells and chondrocytes. Based on our in vitro data, we hypothesized that in vivo treatment with glucocorticoids may diminish the proliferation of tendon and cartilage cells by increasing apoptosis and suppressing the proliferation. Our findings suggest that Dexa could be used with caution in dogs with articular or tendon problems.

scholarly journals CCL22 is a potential bio-marker for osteoarthritic pain and cartilage degeneration

2016 ◽  
Vol 24 ◽  
pp. S75-S76
Author(s):  
G. Ren ◽  
P. Railton ◽  
J.L. Whittaker ◽  
C. Leonard ◽  
P.T. Salo ◽  
...  
Keyword(s):  
Cartilage Degeneration ◽  
Osteoarthritic Pain ◽  
And Cartilage
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