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Osteoclasts (OCs) are key cells affecting bone remodeling, whose differentiation is regulated by various factors including reactive oxygen species (ROS). ROS, intermediate products of the reduction-oxidation reaction during the conversion of oxygen to water, promote osteoclast differentiation by activating NF-κB, MAPK and AKT signaling pathways, downstream of RANKL/RANK signaling pathway. In recent years, a variety of novel antioxidants show targeted effects on inhibition of osteoclast differentiation, expected to provide new ideas for the treatment of osteolytic diseases such as osteoporosis. In this paper, it is reviewed that the production and removal of ROS in OCs, the regulation of osteoclast differentiation by ROS and research progress of antioxidants treatment of osteolytic diseases, in order to explore the enormous potential of ROS as the targets for the treatment of osteolytic diseases. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Osteoporosis is the property of Chinese Journal of Osteoporosis and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Diabetes and osteoporosis are systemic chronic metabolic diseases closely related to aging. The decrease of bone strength and low turnover bone metabolism are accompanied by the occurrence and development of diabetes. They have mutually reinforcing phenotypic characteristics, i.e., metabolic disorders caused by aging, high glucose, and hypoxia, leading to the occurrence of diabetic osteoporosis. The essence of aging is the decline of antioxidant capacity of the body. High glucose induction not only accelerates the aging process of all kinds of cells, but also causes oxidative stress by increasing the level of reactive oxygen species in cell mitochondria and by destroying the dynamic balance of cell mitochondria, eventually leads to cell damage. As the co-disease mechanism of diabetes and osteoporosis, hypoxia inducible factor-1α plays an important role in the establishment of diabetic osteoporosis in the hypoxia-hyperglycemia axis. Therefore, the author discusses the oxidative stress mechanism of diabetic osteoporosis based on the hypoxia-hyperglycemia axis in order to provide new ideas for the clinical prevention and treatment of the disease. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Osteoporosis is the property of Chinese Journal of Osteoporosis and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Osteoporosis（ OP） is a metabolic bone disorder characterized by low bone mass, loss of microstructure, increased brittleness, and advanced fracture. In recent years, researches on the prevention and treatment of osteoporosis in traditional Chinese medicine have been continuously deepening. It has been found that isopsoralen promotes bone formation, inhibits bone absorption, and improves chondrocyte status, which has the potential to become an effective drug in the treatment of OP. Combined with relevant studies, this paper summarizes the effect of isopsoralen on bone metabolism, chondrocytes, and OP animal models, and discusses the safety of the drug, so as to provide data for the subsequent development of isopsoralen. [ABSTRACT FROM AUTHOR]

Objective To observe the methylation level of leptin promoter in bone of ovariectomized osteoporosis rats, and to explore the molecular mechanism of reinforcing kidney to strengthen bone Chinese herbal compound in preventing and treating postmenopausal osteoporosis (PMOP). Methods PMOP model was established by ovariectomy in Wistar rats. Rats were divided into 4 groups: normal group, model group, reinforcing kidney to strengthen bone Chinese herbal compound group, and Xianlinggubao positive control group. After 14 weeks of drug administration, bone mineral density was detected with X-ray absorptiometry. Micro-morphology structure of HE stained paraffin section of the femoral head was observed with the microscope. Leptin promoter methylation level was detected with MassARRA Y. Results (1) Bone mineral density of the lumbar vertebrae 1- 6 decreased significantly in model group compared to that in normal group (P< 0. 01) and increased significantly in reinforcing kidney to strengthen bone Chinese herbal compound group and Xianlinggubao positive control group compared to that in model group (P

Objective To explore the therapeutic mechanism of kidney-reinforcing traditional Chinese medicine compound on ovariectomized osteoporosis rats based on methylation level of Dlx5 promoter in bone. Methods Postmenopausal osteoporosis(PMOP) rat model was established with ovariectomy. All the rats were divided into 4 groups: normal group,model group, kidneyreinforcing traditional Chinese medicine compound group, and Xianlinggubao positive control group. After 14 weeks of drug administration, bone mineral density was detected using X-ray absorptiometry. Dlx5 promoter methylation level was detected using MassARRAY. Results(1) Compared to those in normal group,bone mineral density of the lumbar vertebra 1-6 in model group decreased significantly(P<0.01),and the methylation level of Dlx5 promoter-470 bp--4 bp CpG2. 3 increased significantly in bone(P<0.01).(2) Bone mineral density of the lumbar vertebra 1-6 in kidney-reinforcing traditional Chinese medicine compound group and Xianlinggubao positive control group increased significantly(P<0. 05), and the methylation level of Dlx5 promoter-470 bp--4 bp CpG1 decreased significantly in bone(P < 0.05),compared with those in model group. Conclusion Kidneyreinforcing traditional Chinese medicine compound prevents and interferes with PMOP effectively through the epigenetic mechanism of reducing Dlx5 promoter methylation level in bone. [ABSTRACT FROM AUTHOR]

Objective To study the effects of isopsoralen on bone marrowmesenchymal stem cells (BMSCs) of mice with ovariectomized osteoporosis and to explore the relevant mechanisms. Methods Eighteen C57 / BL6 female rats were randomly divided into sham operation group (sham), ovariectomized group (OVX) and ovariectomized plus isopsoralen group (OVX +ISO), with 6 rats in each group. In the OVX group and OVX + ISO group, surgery was performed from the back of the proximal iliac spine muscle, and bilateral ovaries were removed and the bilateral fallopian tubes cut off after the ligation of the upper fallopian tube. In the Sham group, part of the fat tissue around the ovary was removed after the same procedure. All rats of the OVX + ISO group was gavaged isopsoralen at a dose of 20 mg/(kg·d) for two months began 5 days before the removal of ovaries. All of the rats in the sham group were gavaged with equal dose of normal saline. After 12 weeks,rats were sacrificed to evaluate the quality of fat cells in the bone marrowcavity. Bone mass of femur was evaluated by micro-CT scan and RUNX2 and PPAR-γ were also assessed. Results Isopsoralen can significantly decrease the increase in fat cells resulted from ovariectomized in OVX mice. In addition, isopsoralen treatment can significantly reduce the loss of bone mass due to ovariectomized in the lower femur. Trabecular bone thickness (TB. Th), bone volume / total volume (BV / TV) and trabecular number (TB. N) were all significant greater (P< 0. 05) in the OVX + ISO group than those in the OVX group; and bone trabecular separation (TB. SP) was significant lower (P< 0. 05) in the OVX + ISO group than that in the OVX group. The Runx2 and PPAR-γ immune fluorescence tips in the lower femur of C57 / BL6 mice showed that isopsoralen treatment could increase Runx2 expression that was decreased due to ovariectomy, and inhibit increased expression of PPAR-γ, namely the immune fluorescence expression intensities of Runx2 and PPAR-γ in lower femur were significant higher in the OVX + ISO group than that of OVX group (P < 0. 05). Conclusion Study the effects and mechanisms of isopsoralen treatment on BMSCs in ovariectomized mice provides a newavenue for the treatment of osteoporosis. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Osteoporosis is the property of Chinese Journal of Osteoporosis and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)