Notoginseng Radix and Rehmanniae Radix Preparata Extract Combination (YH23537) Reduces Pain and Cartilage Degeneration in Rats with Monosodium Iodoacetate-Induced Osteoarthritis

2018 ◽  
Vol 21 (8) ◽  
pp. 745-754 ◽  
Author(s):  
Joo Yeon Jhun ◽  
Hyun Sik Na ◽  
Jang Woo Shin ◽  
Kyung Ah Jung ◽  
Hyeon Beom Seo ◽  
...  
2014 ◽  
Vol 14 (1) ◽  
pp. 45 ◽  
Author(s):  
Su-Jin Moon ◽  
Jeong-Hee Jeong ◽  
Joo Yeon Jhun ◽  
Eun Ji Yang ◽  
Jun-Ki Min ◽  
...  

2020 ◽  
Vol 98 (11) ◽  
pp. 763-770
Author(s):  
Hamza Malik Okuyan ◽  
Menderes Yusuf Terzi ◽  
İhsan Karaboğa ◽  
Serdar Doğan ◽  
Aydıner Kalacı

Osteoarthritis (OA) is a degenerative disease affecting the majority of over 65 year old people and characterized by cartilage degeneration, subchondral abnormal changes, and inflammation. Despite the enormous socioeconomic burden caused by OA, currently, there is no effective therapy against it. Upper zone of growth plate and cartilage matrix associated protein (UCMA) is a vitamin K dependent protein and has a critical role in pathophysiological conditions associated with bone and cartilage. However, there is no research on the protective role of intra-articular UCMA treatment in OA pathogenesis. Therefore, we aimed to investigate the potential therapeutic role of UCMA in an in vivo model of OA. We report for the first time that intra-articular UCMA injection ameliorated cartilage degeneration in a monosodium iodoacetate induced OA rat model. Furthermore, the OA-induced activation of nuclear factor kappa B and bone morphogenetic protein 2 signals was attenuated by UCMA. Our results indicated that UCMA decreased cartilage oligomeric matrix protein levels but did not affect interleukin 6, total antioxidant status, and total oxidant status levels in the serum. In conclusion, UCMA exhibited a therapeutic potential in the treatment of OA. This protective effect of UCMA is possibly achieved by reducing the aggrecanase activity and the production of inflammatory cytokines.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yan Zhou ◽  
Jianghua Ming ◽  
Yaming Li ◽  
Bochun Li ◽  
Ming Deng ◽  
...  

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.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Wei Lin ◽  
Huijun Kang ◽  
Yike Dai ◽  
Yingzhen Niu ◽  
Guangmin Yang ◽  
...  

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.


Author(s):  
Kazuhiko Hashimoto ◽  
Yutaka Oda ◽  
Koichi Nakagawa ◽  
Terumasa Ikeda ◽  
Kazuhiro Ohtani ◽  
...  

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.


2018 ◽  
Vol 39 (8) ◽  
pp. 908-915 ◽  
Author(s):  
Tomoyuki Nakasa ◽  
Yasunari Ikuta ◽  
Mikiya Sawa ◽  
Masahiro Yoshikawa ◽  
Yusuke Tsuyuguchi ◽  
...  

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.


2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Yu Chen ◽  
Jiuheng Lv ◽  
Yejuan Jia ◽  
Ruiqing Wang ◽  
Zidi Zhang ◽  
...  

In this study, a knee osteoarthritis (KOA) rat model induced by monosodium iodoacetate (MIA) was used to study the effect of moxibustion on improving knee cartilage damage and its effect on the intestinal flora. The experimental rats were divided into the normal group (N), model group (M), moxibustion treatment group (MS), and diclofenac sodium treatment group (DS). After 4 weeks, cartilage pathological damage in the knee joint was evaluated using hematoxylin-eosin and safranin O-fast green staining analysis. ELISAs and Western blots were used to detect the expression levels of IL-1β and TNF-α in the serum and cartilage, respectively. The total DNA of the fecal samples was extracted and subjected to high-throughput sequencing of the V3-V4 region of the 16S rRNA gene to analyze the changes in the intestinal flora. In the model group, the cartilage was obviously damaged, the expression levels of IL-1β and TNF-α in the serum and cartilage were increased, and the abundance and diversity of the intestinal flora were decreased. Moxibustion treatment significantly improved the cartilage damage and reduced the concentration of inflammatory factors in the serum and cartilage. The high-throughput sequencing results showed that compared to the model group, the moxibustion treatment regulated some specific species in the intestinal microorganisms rather than the α diversity. In conclusion, our findings suggest that moxibustion treatment may work through two aspects in rats. On one hand, it directly acts on knee cartilage to promote repair, and on the other hand, it regulates the composition of the intestinal flora and reduces the production of inflammatory factors.


2005 ◽  
Vol 52 (12) ◽  
pp. 3713-3717 ◽  
Author(s):  
Jukka Morko ◽  
Riku Kiviranta ◽  
Kirsi Joronen ◽  
Anna-Marja Säämänen ◽  
Eero Vuorio ◽  
...  

Neuropeptides ◽  
2017 ◽  
Vol 65 ◽  
pp. 56-62 ◽  
Author(s):  
Colombe Otis ◽  
Martin Guillot ◽  
Maxim Moreau ◽  
Johanne Martel-Pelletier ◽  
Jean-Pierre Pelletier ◽  
...  

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