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18 results on '"Zhao, Kangxian"'

4. Tinkering with Tasks Knows No Bounds: ESL Teachers' Adaptations of Task-Based Language-Teaching

Author

Plews, John L. and Zhao, Kangxian

Abstract

Research on implementing task-based language-teaching (TBLT) shows that adapting TBLT in ways that are inconsistent with its principles is common among nonnative-speaker English-as-a-foreign-language teachers. Our study of Canadian native-speaker English-as-a-second language teachers reveals how they also adapt TBLT in ways that are incongruent with its theoretical underpinnings, turning it into Presentation-Practice-Production. We thus question speaker identity as an indicator of a teacher's propensity to adapt TBLT and call for professional development on the effective practice of TBLT for all English-language teachers regardless of their speaker identities.

Published
2010

5. Pristimerin Inhibits Osteoclast Differentiation and Bone Resorption in vitro and Prevents Ovariectomy-Induced Bone Loss in vivo

Author

Sun, Peng, Yang, Qichang, Wang, Yanben, Peng, Jiaxuan, Zhao, Kangxian, Jia, Yewei, Zhang, Tan, Lu, Xuanyuan, Han, Weiqi, and Qian, Yu

Subjects
MAP Kinase Signaling System, Ovariectomy, Osteoclasts, Mice, Osteogenesis, Animals, Humans, Bone Resorption, Osteoporosis, Postmenopausal, Original Research, Drug Design, Development and Therapy, Bone Density Conservation Agents, Dose-Response Relationship, Drug, NFATC Transcription Factors, AKT, Macrophages, Cell Differentiation, X-Ray Microtomography, osteoporosis, Mice, Inbred C57BL, ERK, osteoclast, Female, JNK, Pri, Pentacyclic Triterpenes, Signal Transduction
Abstract

Peng Sun,1,2 Qichang Yang,1 Yanben Wang,2 Jiaxuan Peng,3 Kangxian Zhao,1 Yewei Jia,2 Tan Zhang,2 Xuanyuan Lu,2 Weiqi Han,2 Yu Qian1,2 1The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, People’s Republic of China; 2Department of Orthopedics, Shaoxing People’s Hospital (Shaoxing Hospital, Zhejiang University School of Medicine), Shaoxing, Zhejiang 312000, People’s Republic of China; 3Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi 530021, People’s Republic of ChinaCorrespondence: Yu QianThe Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, No. 109, XueYuan Road, Wenzhou, Zhejiang 325000, People’s Republic of ChinaEmail doctor120@hotmail.comIntroduction: Osteoporosis is a metabolic bone disease characterized by reduced bone quantity and microstructure, typically owing to increased osteoclastogenesis and/or enhanced osteoclastic bone resorption, resulting in uncontrolled bone loss, which primarily affects postmenopausal women. In consideration of the severe side effects of current drugs for osteoporosis, new safe and effective medications are necessary. Pristimerin (Pri), a quinone methide triterpene extracted from Celastraceae and Hippocrateaceae members, exhibits potent antineoplastic and anti-inflammatory effects. However, its effect on osteoclasts remains unknown.Materials and Methods: We evaluated the anti-osteoclastogenic and anti-resorptive effect of Pri on bone marrow-derived osteoclasts and its underlying mechanism in vitro. In addition, the protective effect of Pri on ovariectomy model was also explored in vivo.Results: In vitro, Pri inhibited osteoclast differentiation and mature osteoclastic bone resorption in a time- and dose-dependent manner. Further, Pri suppressed the expression of osteoclast-related genes and the activation of key proteins. Pri also inhibited the early activation of ERK, JNK MAPK, and AKT signaling pathways in bone marrow-derived macrophages (BMMs), ultimately inhibiting the induction and activation of the crucial osteoclast transcriptional factor nuclear factor of activated T‐cell cytoplasmic 1 (NFATc1). In vivo, consistent with our in vitro data, Pri clearly prevented ovariectomy-induced bone loss.Conclusion: Our data showed that Pri inhibits the differentiation and activation of osteoclasts in vitro and in vivo, and could be a promising candidate for treating osteoporosis.Keywords: osteoclast, osteoporosis, ERK, JNK, AKT, Pri

Published
2020

7. Sarsasapogenin Suppresses RANKL-Induced Osteoclastogenesis in vitro and Prevents Lipopolysaccharide-Induced Bone Loss in vivo

Author

Peng, Jiaxuan, Zhao, Kangxian, Zhu, Jiling, Wang, Yanben, Sun, Peng, Yang, Qichang, Zhang, Tan, Han, Weiqi, Hu, Wenjun, Yang, Wanlei, Ruan, Jianwei, and Qian, Yu

Subjects
musculoskeletal diseases, Lipopolysaccharides, Male, Drug Design, Development and Therapy, Dose-Response Relationship, Drug, RANK Ligand, Molecular Conformation, NFATc1, Osteoclasts, Osteolysis, sarsasapogenin, MAPK, NF-κB, Mice, Inbred C57BL, Mice, Structure-Activity Relationship, Osteogenesis, osteoclast, therapeutics, Spirostans, Animals, osteoclastogenesis, Cells, Cultured, Original Research
Abstract

Jiaxuan Peng,1,* Kangxian Zhao,2,* Jiling Zhu,3,* Yanben Wang,4,5 Peng Sun,2 Qichang Yang,2 Tan Zhang,4 Weiqi Han,4 Wenjun Hu,4 Wanlei Yang,4 Jianwei Ruan,6 Yu Qian1,2,4 1Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Guangxi 530021, People’s Republic of China; 2The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, People’s Republic of China; 3Department of Clinical Medicine, Medical College of Shaoxing University, Shaoxing, Zhejiang 312000, People’s Republic of China; 4Department of Orthopaedics, Shaoxing People’s Hospital, Zhejiang University School of Medicine, Shaoxing 312000, Zhejiang, People’s Republic of China; 5Department of Orthopaedics, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, People’s Republic of China; 6Department of Orthopaedics, Taizhou Municipal Hospital, Taizhou 318000, Zhejiang, Republic of China*These authors contributed equally to this workCorrespondence: Yu QianDepartment of Orthopaedics, Shaoxing People’s Hospital, Zhejiang University School of Medicine, Shaoxing 312000, Zhejiang, People’s Republic of ChinaEmail doctor120@hotmail.comIntroduction: Osteoclasts are giant polynuclear cells; their main function is bone resorption. An increased number of osteoclasts and enhanced bone resorption exert significant effects on osteoclast-related bone-lytic diseases, including osteoporosis. Given the limitations of current therapies for osteolytic diseases, it is urgently required to develop safer and more effective alternatives. Sarsasapogenin, a major sapogenin from Anemarrhena asphodeloides Bunge, possesses potent antitumor effects and inhibits NF-κB and MAPK signaling. However, the manner in which it affects osteoclasts is unclear.Methods: We investigated the effects of anti-osteoclastogenic and anti-resorptive of sarsasapogenin on bone marrow-derived osteoclasts.Results: Sarsasapogenin inhibited multiple RANKL-induced signaling cascades, thereby inhibiting the induction of key osteoclast transcription factor NFATc1. The in vivo and in vitro results were consistent: sarsasapogenin treatment protected against bone loss in a mouse osteolysis model induced by lipopolysaccharide.Conclusion: Our research confirms that sarsasapogenin can be used as a new treatment for osteoclast-related osteolytic diseases.Keywords: sarsasapogenin, osteoclast, osteoclastogenesis, NF-κB, MAPK, NFATc1, therapeutics

Published
2020

15. Garcinol suppresses RANKL‐induced osteoclastogenesis and its underlying mechanism.

Author

Jia, Yewei, Jiang, Jiawei, Lu, Xuanyuan, Zhang, Tan, Zhao, Kangxian, Han, Weiqi, Yang, Wanlei, and Qian, Yu

Subjects
GARCINOL, OSTEOCLASTOGENESIS, BONE resorption, OSTEOPOROSIS, LIPOPOLYSACCHARIDES
Abstract

Osteoclasts (OCs) are multinuclear giant cells responsible for bone resorption, and an excessive bone resorption by OCs plays an important role in osteoporosis. Commonly used drugs for the treatment of osteoporosis have severe side effects. As such, identification of alternative treatments is essential. Garcinol, a polyisoprenylated benzophenone extracted from the fruit of Garcinia indica, has shown a strong antitumor effect through the nuclear factor‐κB (NF‐κB) and mitogen‐associated protein kinases (MAPK) signaling pathways. However, the role of garcinol in the osteoclastogenesis is still unclear. Here, we demonstrated that garcinol can inhibit the receptor activator of NF‐κB ligand (RANKL)‐induced osteoclastogenesis, osteoclastogenesis‐related gene expression, the f‐actin ring, and resorption pit formation. In addition, garcinol abrogated RANKL‐induced osteoclastogenesis by attenuating the degradation of the MAPK, NF‐κB, and PI3K‐AKT signaling pathway as well as downstream factors c‐jun, c‐fos, and NFATC1. In vivo, suppression of osteoclastogenesis by garcinol was evidenced by marked inhibition of lipopolysaccharide‐induced bone resorption. In conclusion, our data demonstrated that garcinol inhibited the RANKL‐induced osteoclastogenesis by suppressing the MAPK, NF‐κB, and PI3K‐AKT signaling pathways and thus has potential as a novel therapeutic option for osteolytic bone diseases. Garcinol suppresses osteoclast (OCs) formation and function in vitro. Garcinol impairs the receptor activator for the nuclear factor‐κB ligand (RANKL)‐induced mitogen‐associated protein kinases (MAPK), nuclear factor‐κB (NF‐κB), and AKT signaling pathway. Garcinol suppresses osteolysis in vivo. Garcinol may be a new therapeutic option for osteolytic bone diseases [ABSTRACT FROM AUTHOR]

Published
2019
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16. Deguelin inhibits RANKL‐induced osteoclastogenesis in vitro and prevents inflammation‐mediated bone loss in vivo.

Author

Zhang, Tan, Zhao, Kangxian, Han, Weiqi, Yang, Wanlei, Lu, Xuanyuan, Liu, Qian, Li, Xiucheng, and Qian, Yu

Subjects
*OSTEOCLASTOGENESIS, *OSTEOCLASTS, *BONE diseases, *OSTEOPOROSIS, *ANTINEOPLASTIC agents
Abstract

Excessive bone resorption by osteoclasts (OCs) plays an important role in lytic bone diseases, such as osteoporosis. Although the pharmacological treatment of osteoporosis has been extensively developed, alternative treatments are still needed. Deguelin, a rotenoid isolated from several plant species, is a strong antitumor agent; however, its effect on OCs remains unclear. To the best of our knowledge, this is the first study to report that deguelin inhibits the receptor activator of nuclear factor‐κB (NF‐κB) ligand (RANKL)‐induced osteoclastogenesis, messenger RNA expression of osteoclastic‐specific genes, and osteoclastic bone resorption, in primary bone marrow‐derived macrophages. At the molecular level, deguelin markedly blocked RANKL‐induced osteoclastogenesis by attenuating the phosphorylation of NF‐κB p65 and inhibiting p65 nuclear translocation. In addition, deguelin suppressed the downstream expression of nuclear factor of activated T‐cell cytoplasmic 1, which is a crucial transcription factor in OC differentiation. Consistent with the in vitro results, deguelin inhibited lipopolysaccharide‐induced bone resorption by suppressing osteoclastogenesis. Taken together, our findings reveal that deguelin has antiosteoclastic effects in vitro and in vivo and possesses potential as a new therapeutic option for osteolytic bone diseases. Deguelin suppresses osteoclast formation and function in vitro. Deguelin impairs the receptor activator of nuclear factor‐κB (NF‐κB) ligand (RANKL)‐induced NF‐κB signaling pathway. Deguelin suppresses osteolysis in vivo. Deguelin may be used for treating osteoclast‐related diseases. [ABSTRACT FROM AUTHOR]

Published
2019
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