7 results on '"Ma, Jinzhong"'
Search Results
2. Oxymatrine exerts protective effects on osteoarthritis via modulating chondrocyte homoeostasis and suppressing osteoclastogenesis.
- Author
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Jiang, Yafei, Sang, Weilin, Wang, Cong, Lu, Haiming, Zhang, Tao, Wang, Zhuoying, Liu, Yu, Xue, Bao, Xue, Song, Cai, Zhengdong, Hua, Yingqi, Zhu, Libo, and Ma, Jinzhong
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OSTEOARTHRITIS ,HOMEOSTASIS ,ARTICULAR cartilage diseases ,CARTILAGE cells ,ANTI-inflammatory agents - Abstract
Abstract: Osteoarthritis (OA) is a common degenerative disease characterized by the progressive destruction both articular cartilage and the subchondral bone. The agents that can effectively suppress chondrocyte degradation and subchondral bone loss are crucial for the prevention and treatment of OA. Oxymatrine (OMT) is a natural compound with anti‐inflammatory and antitumour properties. We found that OMT exhibited a strong inhibitory effect on LPS‐induced chondrocyte inflammation and catabolism. To further support our results, fresh human cartilage explants were treated with LPS to establish an ex vivo degradation model, and the results revealed that OMT inhibited the catabolic events of LPS‐stimulated human cartilage and substantially attenuated the degradation of articular cartilage ex vivo. As subchondral bone remodelling is involved in OA progression, and osteoclasts are a unique cell type in bone resorption, we investigated the effects of OMT on osteoclastogenesis, and the results demonstrated that OMT suppresses RANKL‐induced osteoclastogenesis by suppressing the RANKL‐induced NFATc1 and c‐fos signalling pathway in vitro. Further, we found that the anti‐inflammatory and anti‐osteoclastic effects of oxymatrine are mediated via the inhibition of the NF‐κB and MAPK pathways. In animal studies, OMT suppressed the ACLT‐induced cartilage degradation, and TUNEL assays further confirmed the protective effect of OMT on chondrocyte apoptosis. MicroCT analysis revealed that OMT had an attenuating effect on ACLT‐induced subchondral bone loss in vivo. Taken together, these results show that OMT interferes with the vicious cycle associated with OA and may be a potential therapeutic agent for abnormal subchondral bone loss and cartilage degradation in osteoarthritis. [ABSTRACT FROM AUTHOR]
- Published
- 2018
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3. Articular cartilage changes
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Ma Jinzhong and Sang Weilin
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musculoskeletal diseases ,Cartilage, Articular ,medicine.medical_treatment ,chemistry.chemical_element ,Articular cartilage ,Osteoarthritis ,Calcium ,Bone grafting ,law.invention ,law ,medicine ,Animals ,Orthopedics and Sports Medicine ,Hyaline ,Cement ,Bone Transplantation ,business.industry ,Cartilage ,Anatomy ,medicine.disease ,Tibial Fractures ,medicine.anatomical_structure ,Treatment Outcome ,chemistry ,Surgery ,Rabbits ,Electron microscope ,business - Abstract
The morphologic changes of articular cartilage with bone grafting to fill subchondral bone defects were studied in 23-month-old New Zealand rabbits with bilateral tibial subchondral bone defects. The defects were made approximately 5 mm below the articular surface and were covered with surrounding tissues. The right side was filled with calcium sulfate bone graft, and the left side was filled with acrylic cement as control. The articular cartilage above the fillers was harvested 12 weeks postoperatively. Gross observation, histological examination, and transmission electron microscope observation were undertaken. The results showed that cartilage above the calcium sulfate had a normal hyaline articular cartilage appearance. In contrast, cartilage above the acrylic cement showed degenerative changes in both histological and electron microscope observation. These results suggest that using calcium sulfate bone graft to fill subchondral metaphyseal bone defects has no harmful effect to overlying articular cartilage. This substitute can reduce the possibility of osteoarthritis compared to acrylic cement.
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- 2009
4. CDK9 attenuation exerts protective effects on catabolism and hypertrophy in chondrocytes and ameliorates osteoarthritis development.
- Author
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Xue, Song, Zhu, Libo, Wang, Cong, Jiang, Yafei, Lu, Haiming, Liu, Yu, Shao, Qing, Xue, Bao, Sang, Weilin, and Ma, Jinzhong
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CYCLIN-dependent kinases , *ANTERIOR cruciate ligament , *ARTICULAR cartilage , *HYPERTROPHY , *METABOLISM , *CARTILAGE - Abstract
Osteoarthritis (OA) is generally considered to be characterized by progressive articular cartilage destruction. Increasing evidence demonstrates that CDK9, which is a member of cyclin-dependent kinase family, plays a significant role in the regulation of acute and chronic inflammatory diseases. IL-1β, a major proinflammatory cytokine, was used to establish a model of OA in vitro after stimulating chondrocytes. We found that CDK9 was highly expressed in in vitro and in vivo models of inflammation. The role of LDC000067 (abbreviated as LDC067), a specific inhibitor of CDK9, in protecting articular cartilage from immune response has not been fully clarified. Intriguingly, in this study, we demonstrated that LDC067 prevented IL-1β-induced production of metalloproteinases (MMPs) and inflammatory cytokines, including MMP3, MMP9, MMP13, IL-6, IL-8 and TNF-ɑ. Furthermore, we revealed that LDC067 inhibited IL-1β-induced NF-κB signaling pathway activation in chondrocytes. The inhibition of CDK9 could also delay cartilage degeneration in an anterior cruciate ligament transection (ACLT) mouse model in vivo. Taken together, these results highlighted the significance of this CDK9 inhibitor in preventing cartilage destruction and indicated that LDC067 might serve as a potential therapeutic agent for OA. • CDK9 is upregulated in osteoarthritis cartilage and is correlated with the severity of OA. • The specific inhibitor of CDK9, LDC067 attenuates the catabolism and hypertrophic changes of chondrocytes in vitro. • LDC067 suppresses the activation of the NF-κB signaling pathway. • LDC067 ameliorates OA cartilage destruction in vivo and may be a novel therapeutic agent. [ABSTRACT FROM AUTHOR]
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- 2019
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5. BRG1 mediates protective ability of spermidine to ameliorate osteoarthritic cartilage by Nrf2/KEAP1 and STAT3 signaling pathway.
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Mao, Xinjie, Yan, Bing, Chen, Hongjie, Lai, Peng, and Ma, Jinzhong
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SPERMIDINE , *ENDOCHONDRAL ossification , *CELLULAR signal transduction , *CARTILAGE , *POLYAMINES , *ANTERIOR cruciate ligament , *KNEE osteoarthritis - Abstract
[Display omitted] • Spermidine increases BRG1 in osteoarthritic knee cartilage. • BRG1 mediates protective effects of spermidine on osteoarthritic cartilage. • BRG1 regulates Nrf2/KEAP1 and STAT3 signaling pathways, thereby participating in spermidine's ability to improve knee cartilage in osteoarthritis. • Spermidine may be an effective agonist for BRG1 and a potential agent for the treatment of osteoarthritis. Spermidine (SPD) is a natural polyamine that shows beneficial effects on osteoarthritis (OA). However, the effect of SPD on cartilage inflammation remains unknown. This study aimed to investigate the potential mechanisms underlying the protective effect of SPD against OA-induced articular cartilage degradation. SW1353 human chondrocytes were treated with hydrogen peroxide and lipopolysaccharide to induce models of inflammation and oxidative stress, followed by different dose of SPD intervention. Moreover, mice that underwent anterior cruciate ligament transection were bred and treated with SPD. The effects of SPD were observed using a CCK-8 kit, real-time polymerase chain reaction, immunoblotting, and immunofluorescent assays. SPD significantly increased the expression of antioxidant proteins, chondrogenic genes, and inflammatory factors both in vivo and in vitro. And injury of the mouse cartilage was also reduced by SPD. Moreover, SPD activated the Nrf2/KEAP1 pathway and inhibited STAT3 phosphorylation. BRG1 expression was decreased in osteoarthritic mouse cartilage, whereas SPD treatment caused an upregulation. However, when BRG1 was specifically inhibited by an adeno-associated virus and small interfering RNA, the antioxidant and anti-inflammatory effects of SPD were significantly diminished both in vitro and in vivo. We found that SPD ameliorated cartilage damage in OA by activating the BRG1-mediated Nrf2/KEAP1 pathway. SPD and BRG1 may provide new therapeutic options or targets for the treatment of OA. [ABSTRACT FROM AUTHOR]
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- 2023
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6. BRD4 has dual effects on the HMGB1 and NF-κB signalling pathways and is a potential therapeutic target for osteoarthritis.
- Author
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Jiang, Yafei, Zhu, Libo, Zhang, Tao, Lu, Haiming, Wang, Cong, Xue, Bao, Xu, Xun, Liu, Yu, Cai, Zhengdong, Sang, Weilin, Hua, Yingqi, and Ma, Jinzhong
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OSTEOARTHRITIS , *CARTILAGE diseases , *RECEPTOR for advanced glycation end products (RAGE) , *IMMUNOPRECIPITATION , *MATRIX metalloproteinases - Abstract
Osteoarthritis (OA) has traditionally been defined as a non-inflammatory disease. Recently, many studies have demonstrated that OA also has an inflammatory component. BRD4, a member of the Bromodomain and Extra-Terminal Domain family, has emerged as an important regulator of some chronic inflammatory diseases. JQ1, an antagonist of BRD4, modulates transcription of several genes. Our study demonstrated that BRD4 is up-regulated in articular cartilage of OA. BRD4 inhibition attenuated the inflammation and catabolism of chondrocytes and suppressed NF-κB signalling pathway activation. In addition, BRD4 inhibition abolished the transcriptional activity of High Mobility Group Protein B1 (HMGB1). We identified HMGB1 as a direct target of BRD4. Genetic and pharmacological inhibition of BRD4 suppressed IL-1β-induced expression and translocation of HMGB1. Chromatin immunoprecipitation (ChIP) showed the enrichment of BRD4 around the HMGB1 upstream non-promoter region, which diminished with JQ1 treatment. Finally, haematoxylin & eosin and Safranin o/Fast Green staining demonstrated that JQ1 attenuates cartilage destruction in mice with anterior cruciate ligament transection without significant toxic effects. These studies highlighted the importance of BRD4 in the chronic inflammatory reactions of OA, which, as far as we know, was the first report of this finding, and suggested that BRD4 might be a novel potential therapeutic target for the treatment of OA. [ABSTRACT FROM AUTHOR]
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- 2017
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7. Esculentoside A protects against osteoarthritis by ameliorating inflammation and repressing osteoclastogenesis.
- Author
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Shao, Qing, Xue, Song, Jiang, Yafei, Lu, Haiming, Sang, Weilin, Wang, Cong, Xue, Bao, Liu, Yu, Zhu, Libo, and Ma, Jinzhong
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OSTEOCLASTOGENESIS , *CARTILAGE cells , *CHRONIC bronchitis , *INFLAMMATION , *BONE remodeling , *CARTILAGE , *OSTEOARTHRITIS - Abstract
• EsA attenuates inflammation and catabolism of chondrocytes. • EsA restrains RANKL-induced osteoclast formation. • Treatment with EsA suppresses NF-κB and MAPK signalling pathway activation in vitro. • EsA protects OA cartilage in vivo and may be a novel therapeutic target. Osteoarthritis is a relatively common disorder of articular deterioration related to cartilage damage, subchondral bone remodelling, inflammation and metabolism. Agents that can inhibit cartilage degradation and osteoclastogenesis are required for the prevention and treatment of osteoarthritis. Esculentoside A, the highest concentration triterpene saponin isolated from the root of Phytolacca esculenta, has commonly been used for the treatment of chronic bronchitis. However, the role esculentoside A plays in ameliorating osteoarthritis has not been reported. We found that esculentoside A suppresses the expression of IL-1β-induced inflammatory and metabolic factors (IL-6, IL-8, TNF-α, MMP2, MMP3 and MMP13). In addition, esculentoside A restrains osteoclast formation by inhibiting the marker gene expression of NFATc1 and c-Fos. Our results indicate that esculentoside A markedly suppresses IL-1β-induced NF-κB and MAPK signalling pathway activation in chondrocytes, and inhibits RANKL-induced osteoclast precursor generation. Finally, treatment with esculentoside A inhibits the progressive cartilage degeneration and osteoclastogenesis in osteoarthritis mouse models. In summary, these results demonstrate that esculentoside A could be a latent therapeutic reagent for the treatment of osteoarthritis. [ABSTRACT FROM AUTHOR]
- Published
- 2020
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