Biochanin A abrogates osteoclastogenesis in type 2 diabetic osteoporosis via regulating ROS/MAPK signaling pathway based on integrating molecular docking and experimental validation
Abstract Background There are accumulating type 2 diabetes patients who have osteoporosis simultaneously. More effective therapeutic strategies should be discovered. Biochanin A (BCA) has been indicated that can play a role in improving metabolic disorders of type 2 diabetes and preventing osteoporo...
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BMC
2024-01-01
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Series: | BMC Complementary Medicine and Therapies |
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Online Access: | https://doi.org/10.1186/s12906-023-04332-x |
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author | Qi He Junzheng Yang Weijian Chen Zhaofeng Pan Baihao Chen Jiaxu Zeng Nenling Zhang Yuewei Lin Chuyi Chen Jiacong Xiao Miao Li Shaocong Li Haibin Wang Peng Chen |
author_facet | Qi He Junzheng Yang Weijian Chen Zhaofeng Pan Baihao Chen Jiaxu Zeng Nenling Zhang Yuewei Lin Chuyi Chen Jiacong Xiao Miao Li Shaocong Li Haibin Wang Peng Chen |
author_sort | Qi He |
collection | DOAJ |
description | Abstract Background There are accumulating type 2 diabetes patients who have osteoporosis simultaneously. More effective therapeutic strategies should be discovered. Biochanin A (BCA) has been indicated that can play a role in improving metabolic disorders of type 2 diabetes and preventing osteoporosis. But whether BCA can treat type 2 diabetic osteoporosis has not been studied. Purpose To investigate if the BCA can protect against type 2 diabetic osteoporosis and clarify the mechanism. Methods Micro-CT and histology assays were performed to detect the trabecular bone and analyze the bone histomorphology effect of BCA. CCK-8 assay was performed to detect the toxicity of BCA. TRAcP staining, immunofluorescence and hydroxyapatite resorption assay were used to observe osteoclasts differentiation and resorptive activity. Molecular docking provided evidence about BCA regulating the MAPK axis via prediction by the algorithm. QRT-PCR and Western Blotting were utilized to detect the expression of osteoclastogenesis-related markers and MAPK signaling pathway. Results Accumulation of bone volume after BCA treatment could be found based on the 3D reconstruction. Besides, there were fewer osteoclasts in db/db mice treated with BCA than db/db mice treated with saline. In vitro, we found that BCA hadn’t toxicity in osteoclasts precursor, but also inhibited differentiation of osteoclasts. Further, we found that BCA suppresses osteoclastogenesis via ROS/MAPK signaling pathway. Conclusion BCA can prevent type 2 diabetic osteoporosis by restricting osteoclast differentiation via ROS/MAPK signaling pathway. |
first_indexed | 2024-03-08T14:19:15Z |
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institution | Directory Open Access Journal |
issn | 2662-7671 |
language | English |
last_indexed | 2024-03-08T14:19:15Z |
publishDate | 2024-01-01 |
publisher | BMC |
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series | BMC Complementary Medicine and Therapies |
spelling | doaj.art-81de1dc6ce504e35afe8d714989fa0dc2024-01-14T12:11:47ZengBMCBMC Complementary Medicine and Therapies2662-76712024-01-0124111810.1186/s12906-023-04332-xBiochanin A abrogates osteoclastogenesis in type 2 diabetic osteoporosis via regulating ROS/MAPK signaling pathway based on integrating molecular docking and experimental validationQi He0Junzheng Yang1Weijian Chen2Zhaofeng Pan3Baihao Chen4Jiaxu Zeng5Nenling Zhang6Yuewei Lin7Chuyi Chen8Jiacong Xiao9Miao Li10Shaocong Li11Haibin Wang12Peng Chen13First School of Medicine, Guangzhou University of Chinese MedicineThe Laboratory of Orthopaedics and Traumatology of Lingnan Medical Research Center, Guangzhou University of Chinese MedicineFifth School of Medicine, Guangzhou University of Chinese MedicineFirst School of Medicine, Guangzhou University of Chinese MedicineFirst School of Medicine, Guangzhou University of Chinese MedicineFirst School of Medicine, Guangzhou University of Chinese MedicineThe State Key Laboratory of Functions and Applications of Medicinal Plants, School of Pharmaceutical Sciences, Guizhou Medical UniversityFirst School of Medicine, Guangzhou University of Chinese MedicineFirst School of Medicine, Guangzhou University of Chinese MedicineFirst School of Medicine, Guangzhou University of Chinese MedicineFirst School of Medicine, Guangzhou University of Chinese MedicineFirst School of Medicine, Guangzhou University of Chinese MedicineDepartment of Orthopaedics, First Affiliated Hospital, Guangzhou University of Chinese MedicineDepartment of Orthopaedics, First Affiliated Hospital, Guangzhou University of Chinese MedicineAbstract Background There are accumulating type 2 diabetes patients who have osteoporosis simultaneously. More effective therapeutic strategies should be discovered. Biochanin A (BCA) has been indicated that can play a role in improving metabolic disorders of type 2 diabetes and preventing osteoporosis. But whether BCA can treat type 2 diabetic osteoporosis has not been studied. Purpose To investigate if the BCA can protect against type 2 diabetic osteoporosis and clarify the mechanism. Methods Micro-CT and histology assays were performed to detect the trabecular bone and analyze the bone histomorphology effect of BCA. CCK-8 assay was performed to detect the toxicity of BCA. TRAcP staining, immunofluorescence and hydroxyapatite resorption assay were used to observe osteoclasts differentiation and resorptive activity. Molecular docking provided evidence about BCA regulating the MAPK axis via prediction by the algorithm. QRT-PCR and Western Blotting were utilized to detect the expression of osteoclastogenesis-related markers and MAPK signaling pathway. Results Accumulation of bone volume after BCA treatment could be found based on the 3D reconstruction. Besides, there were fewer osteoclasts in db/db mice treated with BCA than db/db mice treated with saline. In vitro, we found that BCA hadn’t toxicity in osteoclasts precursor, but also inhibited differentiation of osteoclasts. Further, we found that BCA suppresses osteoclastogenesis via ROS/MAPK signaling pathway. Conclusion BCA can prevent type 2 diabetic osteoporosis by restricting osteoclast differentiation via ROS/MAPK signaling pathway.https://doi.org/10.1186/s12906-023-04332-xBiochanin AType 2 diabetic osteoporosisOsteoclastsOxidative stressMAPK signaling pathway |
spellingShingle | Qi He Junzheng Yang Weijian Chen Zhaofeng Pan Baihao Chen Jiaxu Zeng Nenling Zhang Yuewei Lin Chuyi Chen Jiacong Xiao Miao Li Shaocong Li Haibin Wang Peng Chen Biochanin A abrogates osteoclastogenesis in type 2 diabetic osteoporosis via regulating ROS/MAPK signaling pathway based on integrating molecular docking and experimental validation BMC Complementary Medicine and Therapies Biochanin A Type 2 diabetic osteoporosis Osteoclasts Oxidative stress MAPK signaling pathway |
title | Biochanin A abrogates osteoclastogenesis in type 2 diabetic osteoporosis via regulating ROS/MAPK signaling pathway based on integrating molecular docking and experimental validation |
title_full | Biochanin A abrogates osteoclastogenesis in type 2 diabetic osteoporosis via regulating ROS/MAPK signaling pathway based on integrating molecular docking and experimental validation |
title_fullStr | Biochanin A abrogates osteoclastogenesis in type 2 diabetic osteoporosis via regulating ROS/MAPK signaling pathway based on integrating molecular docking and experimental validation |
title_full_unstemmed | Biochanin A abrogates osteoclastogenesis in type 2 diabetic osteoporosis via regulating ROS/MAPK signaling pathway based on integrating molecular docking and experimental validation |
title_short | Biochanin A abrogates osteoclastogenesis in type 2 diabetic osteoporosis via regulating ROS/MAPK signaling pathway based on integrating molecular docking and experimental validation |
title_sort | biochanin a abrogates osteoclastogenesis in type 2 diabetic osteoporosis via regulating ros mapk signaling pathway based on integrating molecular docking and experimental validation |
topic | Biochanin A Type 2 diabetic osteoporosis Osteoclasts Oxidative stress MAPK signaling pathway |
url | https://doi.org/10.1186/s12906-023-04332-x |
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