Premium
Tetrahydroxy stilbene glucoside protected against diabetes‐induced osteoporosis in mice with streptozotocin‐induced hyperglycemia
Author(s) -
Zhang Jingjing,
Chen Xiangfan,
Chen Bingbing,
Tong Lijuan,
Zhang Yan
Publication year - 2019
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.6240
Subject(s) - endocrinology , medicine , streptozotocin , rankl , sclerostin , osteoporosis , diabetes mellitus , chemistry , signal transduction , biochemistry , receptor , activator (genetics) , wnt signaling pathway
Tetrahydroxy stilbene glucoside (TSG), an active component from medicinal herb Polygonum multiflorum Thunb, could block the activity of the tissue renin–angiotensin system (RAS), which plays a critical role in development of diabetic osteoporosis. This study aimed to determine if TSG therapy could alleviate bone deteriorations in diabetic mouse model induced by streptozotocin. The diabetic mice showed the loss of trabecular bone mass and the changes of trabecular bone microarchitectural parameters as well as the increase in amount of tartrate‐resistant acid phosphatase (TRAP)–positive osteoclasts at the distal metaphysis of femur when compared with those of nondiabetic mice. Treatment with TSG significantly elevated calcium content in serum and bone and improved biological parameters of trabecular bone, accompanied by increasing messenger RNA (mRNA) expression of RUNX‐2, COL‐I, and OCN and protein expression of β‐catenin as well as down‐regulating protein expression of RAS components including renin and AT1R. In addition, TSG repressed diabetes‐induced decrease in ratio of OPG/RANKL expression and increase in sclerostin expression in bone. The similar effects of TSG on osteoblasts‐specific genes were found in MC3T3‐E1 cells. Taken together, the present study demonstrated the osteopreserve effects of TSG in diabetic mice, and the underlying mechanism might be attributed to its regulation on osteogenesis and osteoclastogenesis.