Salidroside Improves Bone Histomorphology and Prevents Bone Loss in Ovariectomized Diabetic Rats by Upregulating the OPG/RANKL Ratio

Zheng, Hongjian; Qi, Shanshan; Chen, Chen

doi:10.3390/molecules23092398

Cited by 36 publications

(17 citation statements)

References 52 publications

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“…Non-fasting plasma glucose of diabetic mice was higher than that of non-diabetic mice significantly, as well as HbA1c. With regard to body weight of diabetic mice, it was lower than that of non-diabetic mice, similar to previous studies (33, 34). Thus, the diabetic animal model was constructed successfully.…”

Section: Discussionsupporting

confidence: 91%

“…Similar to previous studies, CTX-1, the serum bone resorption marker, was increased in diabetic mice, which may suggest enhanced osteoclast differentiation (35). Interesting, different from bone formation biomarkers in vitro , the expression of ALP, osteocalcin, and PINP in the serum were increased in diabetic mice, which can be explained by the theory that osteoblasts was stimulated to compensate for the insulin depletion-related bone loss (33). The same situation of increased ALP is also found in diabetes patients, which is explained by the matrix hypermineralization (22, 23).…”

Section: Discussionmentioning

confidence: 98%

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Sema3a as a Novel Therapeutic Option for High Glucose-Suppressed Osteogenic Differentiation in Diabetic Osteopathy

Zhang

Zheng

et al. 2019

Front. Endocrinol.

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Objective: Diabetic osteopathy is a common comorbidity of diabetes mellitus, with skeletal fragility, osteoporosis and bone pain. The aim of our study was to highlight the role of sema3a on osteoblast differentiation of MC3T3-e1 in high-glucose condition and explore its therapeutic effect of diabetic osteopathy in vitro and vivo . Methods: In our study, the expression of osteogenesis-related makers, such as ALP, OCN, OPG, β-catenin and Runx2, were analyzed in MC3T3 osteoblastic cells to explore the effect of sema3a on osteoblast differentiation in high-glucose condition, and as was the staining of ALP and Alizarin Red S. In a diabetic animal model, the expression of serum bone metabolic markers, such as ALP, P1NP, OCN, and β-CTX, were analyzed and micro-CT was used to detect bone architecture, including Tb.N, Tb.Th, Tb.Sp, Tb.Pf, BS/BV, and BV/TV after the treatment of sema3a. Results: High glucose significantly inhibited osteogenic differentiation by decreasing the expression of osteogenesis-related makers, sema3a and its receptor of Nrp-1 in a dose-dependent manner in MC3T3. In high-glucose condition, exogenous sema3a (RPL917Mu01) increased the expression of ALP, OCN, OPG, Runx2, β-catenin, and the positive proportion of ALP and Alizarin Red S staining. In addition, in diabetic animal model, exogenous sema3a could increase bone mass and bone mineral density, and downregulate the expression of ALP, P1NP, OCN, and β-CTX. Conclusion: High glucose suppresses osteogenic differentiation in MC3T3 and sema3a may take part in this process. The application of exogenous sema3a alleviates high glucose-induced inhibition of osteoblast differentiation in diabetic osteopathy.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 98%

Sema3a as a Novel Therapeutic Option for High Glucose-Suppressed Osteogenic Differentiation in Diabetic Osteopathy

Zhang

Zheng

et al. 2019

Front. Endocrinol.

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“…It could be divided into bone formation markers and bone resorption markers [32]. ALP, PINP and osteocalcin are bone formation markers representing the metabolic products of osteoblasts activity and bone formation; CTX-1 and TRACP 5b are bone resorption markers, representing the metabolites of osteoclasts activity and bone resorption, especially the degradation products of bone matrix [33]. In this study, both bone formation and bone resorption markers increased in diabetic rats, indicating an accelerated bone turnover in diabetes.…”

Section: Discussionmentioning

confidence: 52%

Chondroitin Sulfate Prevents STZ Induced Diabetic Osteoporosis through Decreasing Blood Glucose, AntiOxidative Stress, Anti-Inflammation and OPG/RANKL Expression Regulation

Zheng

Chen

et al. 2020

IJMS

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Chondroitin sulfate (CS) has antioxidative, anti-inflammatory, anti-osteoarthritic and hypoglycemic effects. However, whether it has antidiabetic osteoporosis effects has not been reported. Therefore, in this study, we established a STZ-induced diabetic rat model; CS (500 mg kg−1 d−1) was orally administrated for eight weeks to study its preventive effects on diabetic osteoporosis. The results showed that eight weeks of CS treatment improved the symptoms of diabetes; the CS-treated group has increased body weight, decreased water or food intake, decreased blood glucose, increased bone-mineral density, repaired bone morphology and decreased femoral osteoclasts and tibia adipocytes numbers. After CS treatment, bone histomorphometric parameters returned to normal, the levels of serum inflammatory cytokines (IL-1β, IL-6 and TNF-α) decreased significantly, serum SOD, GPX and CAT activities increased and MDA level increased. In the CS-treated group, the levels of serum ALP, CTX-1, TRACP 5b, osteocalcin and RANKL decreased and the serum RUNX 2 and OPG levels increased. Bone immunohistochemistry results showed that CS can effectively increase the expression of OPG and RUNX2 and reduce the expression of RANKL in diabetic rats. All of these indicate that CS could prevent STZ induced diabetic osteoporosis—mainly through decreasing blood glucose, antioxidative stress, anti-inflammation and regulation of OPG/RANKL expression. CS can therefore effectively prevent bone loss caused by diabetes.

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“…It is well accepted that the serum specific biomarkers of bone formation (ALP) and bone resorption (TRAP) are widely selected to assess the bone remodeling [ 30 ]. Zheng et al reported that a significantly increased serum ALP levels in the ovariectomized diabetic rats compared with the control [ 31 ], and Liu et al found that a decrease in TRAP level in serum was observed in diabetic rats with Mori Folium treatment [ 32 ]. Intriguingly, we found that the up-regulation of ALP and TRAP were markedly alleviated by LWDH and alendronate (ALN) treatment.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic potential of Liuwei Dihuang pill against KDM7A and Wnt/β-catenin signaling pathway in diabetic nephropathy-related osteoporosis

et al. 2020

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The effects of Liuwei Dihuang Pill (LWDH) on diabetic nephropathy-related osteoporosis (DNOP) are unclear. This study aimed to evaluate the effects of LWDH on KDM7A and Wnt/β-catenin signaling pathway in DNOP rats and the high glucose-induced MC3T3-E1 cells. A DNOP model was prepared by streptozotocin in 9-week old male Sprague-Dawley(SD) rats to evaluate the effects of LWDH. The cell viability and differentiation capacity of high glucose-induced MC3T3-E1 cells were determined by CCK-8 assay, Alizarin Red staining, and alkaline phosphatase (ALP) staining, respectively. Furthermore, the expressions of KDM7A and Wnt1/β-catenin pathway-related proteins were determined by western blot analysis. Treatment of DNOP rats with LWDH could significantly ameliorate the general state, degradation of renal function, and renal pathological changes. LWDH decreased the levels of TNF-α, IL-6, IL-8, IL-1β, ALP, and TRAP, and increased the calcium, phosphorus in serum, as well as decreased the level of the calcium, phosphorus in the urine. Besides, LWDH significantly improved bone mineral density (BMD), bone volume (BV), and the bone microstructure of DNOP rats. Moreover, LWDH increased the levels of the elastic modulus, ultimate load, and bending strength in the femurs. In MC3T3-E1 cells, serum-containing LWDH significantly increases in cell viability and osteoblastic differentiation capability. The expression of α-SMA, vimentin, KDM7A, Wnt1, β-catenin, were significantly down-regulated, and the E-cadherin, H3K9-Me2, H3K27-Me2, BMP-4, BMP-7, Runx2, osteocalcin, and Col1a1 were significantly up-regulated with LWDH treatment. The present study shows that LWDH has a therapeutic effect on DNOP, in part, through down-regulation of KDM7A and Wnt/β-catenin pathway.

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Salidroside Improves Bone Histomorphology and Prevents Bone Loss in Ovariectomized Diabetic Rats by Upregulating the OPG/RANKL Ratio

Cited by 36 publications

References 52 publications

Sema3a as a Novel Therapeutic Option for High Glucose-Suppressed Osteogenic Differentiation in Diabetic Osteopathy

Sema3a as a Novel Therapeutic Option for High Glucose-Suppressed Osteogenic Differentiation in Diabetic Osteopathy

Chondroitin Sulfate Prevents STZ Induced Diabetic Osteoporosis through Decreasing Blood Glucose, AntiOxidative Stress, Anti-Inflammation and OPG/RANKL Expression Regulation

Therapeutic potential of Liuwei Dihuang pill against KDM7A and Wnt/β-catenin signaling pathway in diabetic nephropathy-related osteoporosis

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