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6 results on '"Bengen Zhou"'

1. Cyasterone has a protective effect on steroid-induced Osteonecrosis of the femoral head.

Author

Youqiang Sun, Mengmeng Liang, Yuemeng Xing, Yinfan Duan, Shuangxiao Zhang, Baogui Deng, Xiaobing Xiang, and Bengen Zhou

Subjects
Medicine, Science
Abstract

ContextCyasterone alleviated the apoptosis of BMSCs induced by Dexamethasone via the PI3K/AKT signaling pathway. In addition, Cyasterone had a protective effect on SIONFH model rats by reducing the percentage of empty bone lacunae.ObjectiveTo study the effect of Cyasterone on apoptosis of rat BMSCs and its function on the SIONFH rat model.MethodsRat BMSCs were cultured and divided into Control, DXM and Cyasterone (DXM+Cyasterone) groups. The apoptosis of each group was detected by flow cytometry, the expressions of Caspase-3 and Caspase-9 were detected by immunofluorescence staining, and the mRNA and protein expressions of AKT, BAX, P53, P85, Bcl-2 and Cytochrome C were detected by qPCR and WB. In animal experiments, the femoral head of rats were subjected to HE staining and Micro-CT to observe the necrosis and repair conditions.ResultsThe apoptosis rate of DXM and Cyasterone groups increased compared with Control group, and the apoptosis rate of Cyasterone group decreased compared with DXM group. Compared with DXM group, the mRNA expression of BAX, P53, P85 and Cytochrome C in Cyasterone group were increased, while the protein expression of AKT and Bcl-2 decreased. The histopathological and morphological analysis showed that Cyasterone promoted the trabecular bone structure in rat, which evenly benefit for the repair of SIONFH.ConclusionCyasterone can reduce the apoptosis of rat BMSCs induced by Dexamethasone, and help promoting the bone repair in SIONFH rats.

Published
2023
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2. Tert-butylhydroquinone attenuates osteoarthritis by protecting chondrocytes and inhibiting macrophage polarization

Author

Hua Zhang, Jie Li, Xiaobing Xiang, Bengen Zhou, Changqing Zhao, Qiushi Wei, Youqiang Sun, Jianfa Chen, Boyong Lai, Zequan Luo, and Aihua Li

Subjects
tbhq, osteoarthritis, apoptosis, osteoarthritis (oa), chondrocytes, macrophages, interleukin 6, inflammation, interleukin 1 beta, western blot, blood, destabilization of the medial meniscus (dmm), Diseases of the musculoskeletal system, RC925-935
Abstract

Aims: Tert-butylhydroquinone (tBHQ) has been identified as an inhibitor of oxidative stress-induced injury and apoptosis in human neural stem cells. However, the role of tBHQ in osteoarthritis (OA) is unclear. This study was carried out to investigate the role of tBHQ in OA. Methods: OA animal model was induced by destabilization of the medial meniscus (DMM). Different concentrations of tBHQ (25 and 50 mg/kg) were intraperitoneally injected in ten-week-old female mice. Chondrocytes were isolated from articular cartilage of mice and treated with 5 ng/ml lipopolysaccharide (LPS) or 10 ng/ml interleukin 1 beta (IL-1β) for 24 hours, and then treated with different concentrations of tBHQ (10, 20, and 40 μM) for 12 hours. The expression levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in blood were measured. The expression levels of interleukin 6 (IL-6), IL-1β, and tumour necrosis factor alpha (TNF-α) leptin in plasma were measured using enzyme-linked immunoabsorbent assay (ELISA) kits. The expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathway proteins, and macrophage repolarization-related markers, were detected by western blot. Results: Tert-butylhydroquinone significantly attenuated cartilage destruction in DMM-induced mice in vivo. It demonstrated clear evidence of inhibiting IL-1β-induced chondrocyte apoptosis, inflammation, and differentiation defect in vitro. Meanwhile, tBHQ inhibited LPS-induced activation of NF-κB and MAPK signalling pathways, and also inhibited LPS-induced reactive oxygen species production and macrophages repolarization in vitro. Conclusion: Taken together, tBHQ might be a potential therapeutic strategy for protecting against OA development. Cite this article: Bone Joint Res 2021;10(11):704–713.

Published
2021
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4. Semaphorin 4A acts in a feed-forward loop with NF-κB pathway to exacerbate catabolic effect of IL-1β on chondrocytes

Author

Hao Xiong, Bengen Zhou, Qiushi Wei, Jianfa Chen, Hua Zhang, Fuyifei Liu, Xiaobing Xiang, Qihuo Li, and Jie Li

Subjects
Male, 0301 basic medicine, Interleukin-1beta, Immunology, Inflammation, RAC1, Semaphorins, Pathogenesis, Mice, 03 medical and health sciences, chemistry.chemical_compound, Chondrocytes, 0302 clinical medicine, Downregulation and upregulation, Semaphorin, medicine, Animals, Humans, Immunology and Allergy, Cells, Cultured, Feedback, Physiological, Pharmacology, NF-kappa B, NF-κB, Osteoarthritis, Knee, Cell biology, Mice, Inbred C57BL, IκBα, Cartilage, 030104 developmental biology, chemistry, 030220 oncology & carcinogenesis, Disease Progression, Phosphorylation, medicine.symptom, Signal Transduction
Abstract

Inflammation is fundamental in osteoarthritis (OA) pathogenesis. Semaphorin 4A (Sema4A) has been implicated in immune-associated diseases, however, its role in OA remains unclear. In this study, we show that Sema4A is upregulated in knee OA articular cartilage as well as in chondrocytes exposed to IL-1β treatment in vitro. Moreover, IL-1β-induced Sema4A upregulation is abrogated in the presence of BAY 11-7082, a specific inhibitor of NF-κB pathway, suggesting that the activation of NF-κB is required for Sema4A upregulation under this pathological condition. Intriguingly, Sema4A in turn activates NF-κB through facilitating Rac1/AKT-dependent IκBα phosphorylation and subsequent degradation. Functionally, Sema4A aggravates the catabolic effect of IL-1β on chondrocytes, which can be largely attributed to exacerbated NF-κB activation, since NF-κB inhibition remarkably abolishes this effect. In conclusion, our study suggests that Sema4A is a novel regulator of NF-κB-dependent catabolic events in chondrocytes, which may underlie OA pathogenesis.

Published
2019

5. Network Pharmacology Integrated with Molecular Docking Explores the Mechanisms of Naringin against Osteoporotic Fracture by Regulating Oxidative Stress

Author

Qi Shang, Bengen Zhou, De Liang, You Zhang, Honglin Chen, Xiaobing Jiang, Kai Tang, Xiang Yu, Peng Zhang, Yanchi Gan, Zhida Zhang, Gengyang Shen, Riwei Tan, Hui Ren, Wenhua Zhao, and Guangye Zhu

Subjects
chemistry.chemical_classification, Article Subject, Chemistry, Flavonoid, Peroxisome proliferator-activated receptor, Computational biology, medicine.disease_cause, chemistry.chemical_compound, Other systems of medicine, medicine.anatomical_structure, Complementary and alternative medicine, Osteoclast, medicine, Salt bridge, KEGG, Signal transduction, Naringin, Oxidative stress, RZ201-999, Research Article
Abstract

Naringin (NG), as the most abundant component of Drynariae Rhizoma (Chinese name: Gusuibu), has been proved to be an antioxidant flavonoid on promoting osteoporotic fracture (OF) healing, but relevant research is scanty on the underlying mechanisms. We adopted target prediction, protein-protein interaction (PPI) analysis, Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and molecular docking to establish a system pharmacology database of NG against OF. Totally 105 targets of naringin were obtained, including 26 common targets with OF. A total of 415 entries were obtained through GO Biological Process enrichment analysis ( P < 0.05 ), and 37 entries were obtained through KEGG pathway enrichment analysis with seven signaling pathways included ( P < 0.05 ), which were primarily concerned with p53, IL-17, TNF, estrogen, and PPAR signaling pathways. According to the results of molecular docking, naringin is all bound in the active pockets of the core targets with 3–9 hydrogen bonds through some connections such as hydrophobic interactions, Pi-Pi stacked interactions, and salt bridge, demonstrating that naringin binds tightly to the core targets. In general, naringin may treat OF through multiple targets and multiple pathways via regulating oxidative stress, etc. Notably, it is first reported that NG may regulate osteoclast differentiation and oxidative stress through the expression of the core targets so as to treat OF.

Published
2021

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