1. Jingui Shenqi Pills Regulate Bone-Fat Balance in Murine Ovariectomy-Induced Osteoporosis with Kidney Yang Deficiency
- Author
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Kai Tang, Hui Ren, De Liang, Wenhua Zhao, Weicheng Qin, Zhida Zhang, Qi Shang, Jingjing Tang, Xiaobing Jiang, Honglin Chen, Fuyong Yu, Juanmin Li, Xiang Yu, Xuan Huang, Guifeng Chen, and Gengyang Shen
- Subjects
medicine.medical_specialty ,Article Subject ,Osteoporosis ,Bone morphogenetic protein 2 ,03 medical and health sciences ,chemistry.chemical_compound ,Other systems of medicine ,0302 clinical medicine ,Internal medicine ,Adipocyte ,medicine ,Protein kinase B ,PI3K/AKT/mTOR pathway ,030304 developmental biology ,0303 health sciences ,Kidney ,business.industry ,Osteoblast ,medicine.disease ,FNDC5 ,medicine.anatomical_structure ,Endocrinology ,Complementary and alternative medicine ,chemistry ,030220 oncology & carcinogenesis ,business ,RZ201-999 ,Research Article - Abstract
Jingui Shenqi Pills (JGSQP) have been a staple of traditional Chinese medicine for thousands of years, used primarily as a treatment for kidney yang deficiency (KYD). In vitro analyses of JGSQP revealed strong induction of osteogenic differentiation and inhibition of adipogenic differentiation in bone-marrow-derived mesenchymal stem/stromal cells. However, the mechanisms by which JGSQP regulate the bone-fat balance in murine ovariectomy-induced osteoporosis with KYD have not been reported. Materials and Methods. Two-month-old female C57BL/6 mice were divided randomly into three groups: those receiving a sham operation (Sham); those undergoing bilateral ovariectomy and selection of KYD syndrome (Model); and those subjected to both bilateral ovariectomy and KYD syndrome selection for 8 weeks, followed by JGSQP treatment for 4 weeks (JGSQP). In the Sham and Model groups, mice were given the same dose of distilled water orally for 4 weeks. Animals from all three groups were euthanised at the 12th week. Vertebral microarchitecture and histomorphology were examined by micro-CT and H&E staining, respectively. In addition, we examined the mRNA expression of Akt, Wnt10b, Osterix (Osx), Fndc5, PPARγ, and Fabp4, as well as the protein of AKT, phosphorylation-AKT (p-AKT), BMP2, COL1A1, and FNDC5. Results. JGSQP treatment improved bone microarchitecture and mitigated histomorphological damage relative to the Model group. The osteoblast number (Ob.N/BS) and area (Ob.S/BS) were increased, whereas adipocyte number (adipocyte/tissue area) and area (adipocyte area/tissue area) were decreased in the JGSQP group. JGSQP treatment reduced the mRNA expression of Akt and adipogenesis-related genes (Fndc5, PPARγ, and Fabp4) while promoting osteogenesis-related genes (Wnt10b and Osx) mRNA expression. Additionally, the expression of p-AKT, BMP2, and COL1A1 proteins was increased and FNDC5 protein expression was decreased after JGSQP treatment. Conclusions. JGSQP treatment reversed murine ovariectomy-induced osteoporosis with KYD by controlling bone-fat balance via AKT pathway.
- Published
- 2020