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Application of GPR120 agonist TUG891 to prevention and treatment of osteoporosis

A technology of TUG891, osteoporosis, applied in the application field of GPR120 agonist TUG891 to prevent and treat osteoporosis, to achieve the effects of increasing mineral deposition rate, increasing expression and increasing activity

Active Publication Date: 2014-11-05
FOURTH MILITARY MEDICAL UNIVERSITY
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  • Abstract
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Problems solved by technology

GPR120 is a medium and long-chain unsaturated fatty acid receptor, and its agonist TUG891 plays a role in bone metabolism, such as bone formation and bone healing under osteoporotic conditions, and the regulation of bone marrow mesenchymal stem cell proliferation and differentiation. No report

Method used

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  • Application of GPR120 agonist TUG891 to prevention and treatment of osteoporosis
  • Application of GPR120 agonist TUG891 to prevention and treatment of osteoporosis
  • Application of GPR120 agonist TUG891 to prevention and treatment of osteoporosis

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Embodiment Construction

[0030] The present invention will be described in detail below in conjunction with the accompanying drawings and embodiments, which are explanations rather than limitations of the present invention.

[0031] mBMSC is a mouse bone marrow mesenchymal stem cell that can differentiate into osteoblasts. It is a more commonly used cell model for studying the growth and differentiation of osteoblasts. Under physiological conditions in vivo, mBMSCs can promote the formation and development of osteoblasts and bone growth. one of the important ways. Moreover, the proliferative potential of bone marrow mesenchymal stem cells also plays an important role in the process of bone metabolism and bone remodeling. Fatty acid receptor agonists are commonly used drugs for activating the GPR receptor family in vitro. In order to observe the effect of TUG891 on osteogenic differentiation and cell proliferation, mouse BMSC was selected as the cell model. As an animal model, the ovariectomized (cast...

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Abstract

The invention discloses the application of a GPR120 agonist TUG891 to the prevention and treatment of osteoporosis. High concentration TUG891 has significant osteogenic differentiation promotion effect on bone marrow mesenchymal stem cells, and can significantly improve the proliferation activity of bone marrow mesenchymal stem cells; and a low concentration group cannot ascend osteoblast differentiation and proliferation ability of cells, even partially reduce osteogenic differentiation and proliferation potential. In an ovariectomized mice osteoporosis model, TUG891 can improve microstructure of cancellous bone at the distal femur, and increase the mineral deposition rate at the distal femur, which indicate that TUG891 can promote the proliferation differentiation of bone marrow mesenchymal stem cells to improve bone microstructure and play the role of prevention and treatment of osteoporosis.

Description

technical field [0001] The invention belongs to the technical field of prevention and treatment of osteoporosis, and relates to the application of GPR120 agonist TUG891 in the prevention and treatment of osteoporosis. Background technique [0002] Osteoporosis (Osteoporosis, OP) is a degenerative, systemic, and metabolic bone disease. It is caused by a variety of causes of bone tissue loss, structural changes, and biomechanical decline. It is prone to fractures and poses a serious threat to the elderly. physical and mental health. [0003] With the acceleration of population aging, the proportion of senile osteoporosis in my country is increasing year by year. During the development of osteoporosis, intramedullary fat increases significantly, and the red bone marrow with hematopoietic ability at birth is gradually replaced by yellow bone marrow, and most of the volume of yellow bone marrow is yellow or brown adipose tissue, which is almost full of bone marrow. marrow cavit...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): A61K45/00A61P19/10
Inventor 罗卓荆高博黄强杨柳刘建
Owner FOURTH MILITARY MEDICAL UNIVERSITY
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