Jingui Shenqi Wan alleviates bone loss induced by primary osteoporosis by inhibiting osteoblast pyroptosis
Abstract Objective The primary objective of this study was to elucidate the underlying pharmacological mechanisms by which Jingui Shenqi Wan (JGSQW) alleviates postmenopausal osteoporosis (PMOP). Through a systematic investigation, we sought to identify the specific molecular pathways through which...
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2025-02-01
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Online Access: | https://doi.org/10.1186/s13018-025-05542-4 |
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author | Yuwangxuan Qian Yihe Yu Fan Yang Qixing Liang Dan Xu Jiaxiang Chen Xueqin Hu |
author_facet | Yuwangxuan Qian Yihe Yu Fan Yang Qixing Liang Dan Xu Jiaxiang Chen Xueqin Hu |
author_sort | Yuwangxuan Qian |
collection | DOAJ |
description | Abstract Objective The primary objective of this study was to elucidate the underlying pharmacological mechanisms by which Jingui Shenqi Wan (JGSQW) alleviates postmenopausal osteoporosis (PMOP). Through a systematic investigation, we sought to identify the specific molecular pathways through which JGSQW modulates the progression of PMOP, thereby providing a scientific basis for its clinical application. Methods We established an ovariectomized (OVX) mouse model to simulate estrogen deficiency-induced PMOP. Initially, micro-CT imaging and Alcian blue hematoxylin/orange G (ABH/OG) staining were employed to assess the effects of JGSQW on bone microarchitecture and bone mass preservation. Immunohistochemistry (IHC) was then utilized to evaluate the expression of osteogenic markers, including Osterix (OSX), Runx2, and Osteopontin (OPN). Additionally, Tartrate - Resistant Acid Phosphatase (TRAP) staining was performed to visualize and quantify osteoclasts. We further investigated the potential role of JGSQW in modulating the pyroptosis pathway. Results JGSQW effectively alleviates the destruction of bone microstructure and the loss of bone mass caused by estrogen deficiency, an effect that appears to be mediated by promoting osteogenesis. Additionally, JGSQW significantly downregulates the expression of GSDMD in osteoblasts and mitigates the abnormal release of inflammatory factors, thereby maintaining the normal functional activities of osteoblasts. Conclusion JGSQW may effectively mitigate the progression of estrogen deficiency-induced PMOP by inhibiting the dysregulated activation of osteoblast pyroptosis. |
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institution | Kabale University |
issn | 1749-799X |
language | English |
publishDate | 2025-02-01 |
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spelling | doaj-art-a8c96f38239344969a77fbf0b14714ec2025-02-09T12:47:04ZengBMCJournal of Orthopaedic Surgery and Research1749-799X2025-02-0120111110.1186/s13018-025-05542-4Jingui Shenqi Wan alleviates bone loss induced by primary osteoporosis by inhibiting osteoblast pyroptosisYuwangxuan Qian0Yihe Yu1Fan Yang2Qixing Liang3Dan Xu4Jiaxiang Chen5Xueqin Hu6The Second Clinical Medical College of Zhejiang, Chinese Medical UniversityThe Second Clinical Medical College of Zhejiang, Chinese Medical UniversityThe First Clinical Medical College of Zhejiang, Chinese Medical UniversityZhejiang Chinese Medical UniversityZhejiang Chinese Medical UniversityThe First Clinical Medical College of Zhejiang, Chinese Medical UniversityThe First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine)Abstract Objective The primary objective of this study was to elucidate the underlying pharmacological mechanisms by which Jingui Shenqi Wan (JGSQW) alleviates postmenopausal osteoporosis (PMOP). Through a systematic investigation, we sought to identify the specific molecular pathways through which JGSQW modulates the progression of PMOP, thereby providing a scientific basis for its clinical application. Methods We established an ovariectomized (OVX) mouse model to simulate estrogen deficiency-induced PMOP. Initially, micro-CT imaging and Alcian blue hematoxylin/orange G (ABH/OG) staining were employed to assess the effects of JGSQW on bone microarchitecture and bone mass preservation. Immunohistochemistry (IHC) was then utilized to evaluate the expression of osteogenic markers, including Osterix (OSX), Runx2, and Osteopontin (OPN). Additionally, Tartrate - Resistant Acid Phosphatase (TRAP) staining was performed to visualize and quantify osteoclasts. We further investigated the potential role of JGSQW in modulating the pyroptosis pathway. Results JGSQW effectively alleviates the destruction of bone microstructure and the loss of bone mass caused by estrogen deficiency, an effect that appears to be mediated by promoting osteogenesis. Additionally, JGSQW significantly downregulates the expression of GSDMD in osteoblasts and mitigates the abnormal release of inflammatory factors, thereby maintaining the normal functional activities of osteoblasts. Conclusion JGSQW may effectively mitigate the progression of estrogen deficiency-induced PMOP by inhibiting the dysregulated activation of osteoblast pyroptosis.https://doi.org/10.1186/s13018-025-05542-4JGSQWPostmenopausal osteoporosisPyroptosisOsteoblast |
spellingShingle | Yuwangxuan Qian Yihe Yu Fan Yang Qixing Liang Dan Xu Jiaxiang Chen Xueqin Hu Jingui Shenqi Wan alleviates bone loss induced by primary osteoporosis by inhibiting osteoblast pyroptosis Journal of Orthopaedic Surgery and Research JGSQW Postmenopausal osteoporosis Pyroptosis Osteoblast |
title | Jingui Shenqi Wan alleviates bone loss induced by primary osteoporosis by inhibiting osteoblast pyroptosis |
title_full | Jingui Shenqi Wan alleviates bone loss induced by primary osteoporosis by inhibiting osteoblast pyroptosis |
title_fullStr | Jingui Shenqi Wan alleviates bone loss induced by primary osteoporosis by inhibiting osteoblast pyroptosis |
title_full_unstemmed | Jingui Shenqi Wan alleviates bone loss induced by primary osteoporosis by inhibiting osteoblast pyroptosis |
title_short | Jingui Shenqi Wan alleviates bone loss induced by primary osteoporosis by inhibiting osteoblast pyroptosis |
title_sort | jingui shenqi wan alleviates bone loss induced by primary osteoporosis by inhibiting osteoblast pyroptosis |
topic | JGSQW Postmenopausal osteoporosis Pyroptosis Osteoblast |
url | https://doi.org/10.1186/s13018-025-05542-4 |
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