Qizhi Kebitong Formula Ameliorates Streptozocin-Induced Diabetic Osteoporosis through Regulating the PI3K/Akt/NF-


Journal

BioMed research international
ISSN: 2314-6141
Titre abrégé: Biomed Res Int
Pays: United States
ID NLM: 101600173

Informations de publication

Date de publication:
2022
Historique:
received: 05 03 2022
revised: 22 06 2022
accepted: 15 07 2022
entrez: 1 9 2022
pubmed: 2 9 2022
medline: 8 9 2022
Statut: epublish

Résumé

Diabetic osteoporosis (DOP) is a progressive osteoblast dysfunction induced by high glucose, which has negative impacts on bone homeostasis. Qizhi Kebitong formula (QKF) is a traditional Chinese medicine (TCM) formula for treating DOP. However, its role in the protection of DOP has not been clarified yet. Here, we aimed to explore the potential mechanisms of QKF on DOP development via Network pharmacology was used to detect the key targets and signaling pathways of QKF on DOP. The effects of QKF on DOP were examined by the phenotypic characteristics, micro-CT, and hematoxylin-eosin (H&E) staining. The predicted targets and pathways were validated by a streptozocin- (STZ-) induced mouse model. Subsequently, the levels of the selected genes and proteins were analyzed using qRT-PCR and Western blot. Finally, AutoDock and PyMOL were used for molecular docking. In this study, 90 active compounds and 2970 related disease targets have been found through network pharmacology. And QKF could improve the microstructures of femur bone mass, reduce inflammatory cell infiltration, and downregulate the levels of TNF- Altogether, our findings suggested that QKF could markedly alleviate osteoblast dysfunction by modulating the key targets and PI3K/Akt/NF-

Sections du résumé

Background UNASSIGNED
Diabetic osteoporosis (DOP) is a progressive osteoblast dysfunction induced by high glucose, which has negative impacts on bone homeostasis. Qizhi Kebitong formula (QKF) is a traditional Chinese medicine (TCM) formula for treating DOP. However, its role in the protection of DOP has not been clarified yet. Here, we aimed to explore the potential mechanisms of QKF on DOP development via
Methods UNASSIGNED
Network pharmacology was used to detect the key targets and signaling pathways of QKF on DOP. The effects of QKF on DOP were examined by the phenotypic characteristics, micro-CT, and hematoxylin-eosin (H&E) staining. The predicted targets and pathways were validated by a streptozocin- (STZ-) induced mouse model. Subsequently, the levels of the selected genes and proteins were analyzed using qRT-PCR and Western blot. Finally, AutoDock and PyMOL were used for molecular docking.
Results UNASSIGNED
In this study, 90 active compounds and 2970 related disease targets have been found through network pharmacology. And QKF could improve the microstructures of femur bone mass, reduce inflammatory cell infiltration, and downregulate the levels of TNF-
Conclusion UNASSIGNED
Altogether, our findings suggested that QKF could markedly alleviate osteoblast dysfunction by modulating the key targets and PI3K/Akt/NF-

Identifiants

pubmed: 36046447
doi: 10.1155/2022/4469766
pmc: PMC9420605
doi:

Substances chimiques

Drugs, Chinese Herbal 0
NF-kappa B 0
Streptozocin 5W494URQ81
Proto-Oncogene Proteins c-akt EC 2.7.11.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

4469766

Informations de copyright

Copyright © 2022 Lulu Tian et al.

Déclaration de conflit d'intérêts

The authors declare that there were no conflicts of interest regarding the publication of this paper.

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Auteurs

Lulu Tian (L)

College of Chinese Medicine, Changchun University of Chinese Medicine, 130117, China.

Lu Ding (L)

Jilin Ginseng Academy, Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Ministry of Education, Jilin Provincial Key Laboratory of Bio-Macromolecules of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, 130117 Jilin, China.

Guoqiang Wang (G)

Department of Endocrinology, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun 130021, China.

Yu Guo (Y)

College of Chinese Medicine, Changchun University of Chinese Medicine, 130117, China.

Yunyun Zhao (Y)

College of Chinese Medicine, Changchun University of Chinese Medicine, 130117, China.

Yuchi Wei (Y)

College of Chinese Medicine, Changchun University of Chinese Medicine, 130117, China.

Xingquan Li (X)

College of Chinese Medicine, Changchun University of Chinese Medicine, 130117, China.

Wei Zhang (W)

Jilin Ginseng Academy, Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Ministry of Education, Jilin Provincial Key Laboratory of Bio-Macromolecules of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, 130117 Jilin, China.

Jia Mi (J)

Department of Endocrinology, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun 130021, China.

Xiangyan Li (X)

Jilin Ginseng Academy, Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Ministry of Education, Jilin Provincial Key Laboratory of Bio-Macromolecules of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, 130117 Jilin, China.

Zeyu Wang (Z)

Department of Scientific Research, Changchun University of Chinese Medicine, Changchun, China.

Xiuge Wang (X)

Department of Endocrinology, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun 130021, China.

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Classifications MeSH