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Your search keyword '"Xiong, Sidong"' showing total 22 results
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22 results on '"Xiong, Sidong"'

1. Spider Silk Protein Forms Amyloid‐Like Nanofibrils through a Non‐Nucleation‐Dependent Polymerization Mechanism (Small 46/2023)

Author

Qi, Xingmei, primary, Wang, Yu, additional, Yu, Hairui, additional, Liu, Ruifang, additional, Leppert, Axel, additional, Zheng, Zihan, additional, Zhong, Xueying, additional, Jin, Zhen, additional, Wang, Han, additional, Li, Xiaoli, additional, Wang, Xiuzhe, additional, Landreh, Michael, additional, A. Morozova‐Roche, Ludmilla, additional, Johansson, Jan, additional, Xiong, Sidong, additional, Iashchishyn, Igor, additional, and Chen, Gefei, additional

Published
2023
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3. Bacterial extracellular vesicles: A position paper by the microbial vesicles task force of the Chinese society for extracellular vesicles

Author

Wen, Minghui, primary, Wang, Jingyu, additional, Ou, Zihao, additional, Nie, Guangjun, additional, Chen, Ye, additional, Li, Min, additional, Wu, Zhiwei, additional, Xiong, Sidong, additional, Zhou, Hongwei, additional, Yang, Zifeng, additional, Long, Gang, additional, Su, Jiacan, additional, Liu, Han, additional, Jin, Yingying, additional, Wen, Zhenke, additional, Fu, Yuxuan, additional, Zhou, Tieli, additional, Xie, Hui, additional, Guan, Wenda, additional, Sun, Xi, additional, Wang, Zhang, additional, Wang, Juan, additional, Chen, Xunxun, additional, Jiang, Linglei, additional, Qin, Xiaolin, additional, Xue, Yicong, additional, Huang, Mei, additional, Huang, Xinyue, additional, Pan, Ruoru, additional, Zhen, Haojun, additional, Du, Yuqi, additional, Li, Qianbei, additional, Huang, Xixin, additional, Wu, Yuanyuan, additional, Wang, Pingping, additional, Zhao, Kening, additional, Situ, Bo, additional, Hu, Xiumei, additional, and Zheng, Lei, additional

Published
2023
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16. Kushen flavonoids induce apoptosis in tumor cells by inhibition of NF‐κB activation and multiple receptor tyrosine kinase activities

Author

Han, Jun, primary, Sun, Mingyu, additional, Cui, Yumin, additional, Wang, Tao, additional, Zhang, Weihan, additional, Guo, Mingchuan, additional, Zhou, Yuan, additional, Liu, Wei, additional, Zhang, Meifang, additional, Duan, Jifeng, additional, Xiong, Sidong, additional, Yao, Minghui, additional, and Yan, Xiaoqiang, additional

Published
2007
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21. HMGB1 Promotes Systemic Lupus Erythematosus by Enhancing Macrophage Inflammatory Response.

Author

Lu M, Yu S, Xu W, Gao B, and Xiong S

Subjects
Adult, Animals, Antibodies, Antinuclear blood, Antibodies, Antinuclear immunology, Case-Control Studies, Cell Line, Cytokines metabolism, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Female, Gene Expression, HMGB1 Protein blood, HMGB1 Protein genetics, Humans, Inflammation Mediators metabolism, Lupus Erythematosus, Systemic diagnosis, Lupus Erythematosus, Systemic drug therapy, Male, Middle Aged, Receptor for Advanced Glycation End Products metabolism, Severity of Illness Index, Toll-Like Receptor 2 metabolism, Toll-Like Receptor 4 metabolism, Young Adult, HMGB1 Protein metabolism, Lupus Erythematosus, Systemic immunology, Lupus Erythematosus, Systemic metabolism, Macrophages immunology, Macrophages metabolism
Abstract

Background/Purpose. HMGB1, which may act as a proinflammatory mediator, has been proposed to contribute to the pathogenesis of multiple chronic inflammatory and autoimmune diseases including systemic lupus erythematosus (SLE); however, the precise mechanism of HMGB1 in the pathogenic process of SLE remains obscure. Method. The expression of HMGB1 was measured by ELISA and western blot. The ELISA was also applied to detect proinflammatory cytokines levels. Furthermore, nephritic pathology was evaluated by H&E staining of renal tissues. Results. In this study, we found that HMGB1 levels were significantly increased and correlated with SLE disease activity in both clinical patients and murine model. Furthermore, gain- and loss-of-function analysis showed that HMGB1 exacerbated the severity of SLE. Of note, the HMGB1 levels were found to be associated with the levels of proinflammatory cytokines such as TNF-α and IL-6 in SLE patients. Further study demonstrated that increased HMGB1 expression deteriorated the severity of SLE via enhancing macrophage inflammatory response. Moreover, we found that receptor of advanced glycation end products played a critical role in HMGB1-mediated macrophage inflammatory response. Conclusion. These findings suggested that HMGB1 might be a risk factor for SLE, and manipulation of HMGB1 signaling might provide a therapeutic strategy for SLE.

Published
2015
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22. Kushen flavonoids induce apoptosis in tumor cells by inhibition of NF-kappaB activation and multiple receptor tyrosine kinase activities.

Author

Han J, Sun M, Cui Y, Wang T, Zhang W, Guo M, Zhou Y, Liu W, Zhang M, Duan J, Xiong S, Yao M, and Yan X

Subjects
Animals, Antineoplastic Agents, Phytogenic administration & dosage, Antineoplastic Agents, Phytogenic therapeutic use, Cell Line, Tumor drug effects, Cell Line, Tumor metabolism, Drugs, Chinese Herbal administration & dosage, Drugs, Chinese Herbal therapeutic use, Flavonoids administration & dosage, Flavonoids therapeutic use, Humans, Mice, Mice, Inbred BALB C, NF-kappa B metabolism, Receptor Protein-Tyrosine Kinases metabolism, Transplantation, Heterologous, Antineoplastic Agents, Phytogenic pharmacology, Apoptosis drug effects, Drugs, Chinese Herbal pharmacology, Flavonoids pharmacology, Phytotherapy
Abstract

In this report, the mechanism of the antitumor activities of Kushen flavonoids (KS-Fs) were explored. KS-Fs and kurarinone (Kur), a single flavonoid compound, were able to induce apoptosis of H460 and Eca-109 cells in vitro and H460 cells in vivo. The apoptosis inducing effect was enhanced in the presence of Taxol. In H460 xenograft mice treated with Kur, down-regulation of Bcl-2 and up-regulation of caspase 8 and caspase 3 in tumors were observed by immunohistochemical staining. In addition, KS-Fs and Kur were able to inhibit TNFalpha-induced NF-kappaB activation in 293 cells mediated by the decreased IkappaBalpha phosphorylation. Further the effects of KS-Fs and Kur on multiple receptor tyrosine kinase activities were explored. In cell-based assays, KS-Fs and Kur inhibited the EGF-induced EGF receptor phosphorylation in A431 cells and a constitutively activated Her-2 in MDA-MB-453s cells. In enzymatic assays, KS-Fs and Kur inhibited KDR, but not PDGF BR activities. In A431 xenograft mice treated with Kur, an inhibition of EGF receptor phosphorylation in tumors was observed. These results reveal a novel mechanism by which KS-Fs induces apoptosis in tumors by acting on multiple cellular targets including the inhibition of NF-kappaB activation and multiple receptor tyrosine kinase activities.

Published
2007
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