Chondroitin Sulfate Alleviates Diabetic Osteoporosis and Repairs Bone Microstructure via Anti-Oxidation, Anti-Inflammation, and Regulating Bone Metabolism

Abstract

Diabetic osteoporosis (DOP) belongs to secondary osteoporosis caused by diabetes; it has the characteristics of high morbidity and high disability. In the present study, we constructed a type 1 diabetic rat model and administered chondroitin sulfate (200 mg/kg) for 10 weeks to observe the preventive effect of chondroitin sulfate on the bone loss of diabetic rats. The results showed that chondroitin sulfate can reduce blood glucose and relieve symptoms of diabetic rats; in addition, it can significantly increase the bone mineral density, improve bone microstructure, and reduce bone marrow adipocyte number in diabetic rats; after 10 weeks of chondroitin sulfate administration, the SOD activity level was upregulated, as well as CAT levels, indicating that chondroitin sulfate can alleviate oxidative stress in diabetic rats. Chondroitin sulfate was also found to reduce the level of serum inflammatory cytokines (TNF-α, IL-1, IL-6, and MCP-1) and alleviate the inflammation in diabetic rats; bone metabolism marker detection results showed that chondroitin sulfate can reduce bone turnover in diabetic rats (decreased RANKL, CTX-1, ALP, and TRACP 5b levels were observed after 10 weeks of chondroitin sulfate administration). At the same time, the bone OPG and RUNX 2 expression levels were higher after chondroitin sulfate treatment, the bone RANKL expression was lowered, and the OPG/RANKL ratio was upregulated. All of the above indicated that chondroitin sulfate could prevent STZ-induced DOP and repair bone microstructure; the main mechanism was through anti-oxidation, anti-inflammatory, and regulating bone metabolism. Chondroitin sulfate could be used to develop anti-DOP functional foods and diet interventions for diabetes.

Selected Parameters of Bone Turnover in Neuroendocrine Tumors—A Potential Clinical Use?

“…As it is known, increasing OPG levels inhibit osteoclastogenesis through the mediation of the RANK/RANKL/OPG pathway and might play a role in increasing bone mass [16]. On the contrary, according to Qi et al, in diabetic osteoporosis, it was confirmed that treatment with chondroitin sulfate (which can reduce glucose level) in diabetic rats can increase OPG level and decrease RANKL expression, and in this mechanism may improve the bone microstructure and the bone mineral density [40]. Gohar et al suggested an association between lipids and OPG in a group of patients with depression and schizophrenia.…”

EPDR1 is a noncanonical effector of insulin-mediated angiogenesis regulated by an endothelial-specific TGF-β receptor complex

“…For instance, chondroitin sulfate synthase 2 (44,45) and prostaglandin F2 receptor associated protein (46)(47)(48) are two of the top hits ranked higher than EPDR1 whereas others, including osteopontin (49,50) and platelet-derived growth factor receptor beta (51,52), represent promising candidates ranked slightly lower based on several parameters including fold-changes over negative control and unique peptide counts identified (Figure S3B). Future studies could explore whether these protein factors can serve as unique vascular targets during pathologic angiogenesis such as in diabetic retinopathy (53)(54)(55)(56)(57).…”

“…S3 B ). Future studies could explore whether these protein factors can serve as unique vascular targets during pathologic angiogenesis such as in diabetic retinopathy ( 53 , 54 , 55 , 56 , 57 ).…”

Hydrogen saline water accelerates fracture healing by suppressing autophagy in ovariectomized rats

“…One limitation of this study is that it did not include knockout mice to verify the results, but the treatment of osteoporotic fractures has always been difficult, so the research was still beneficial for the formulation of new treatment strategies. Furthermore, bone turnover, which is considered important for illustrating bone remodeling, as evidenced by cross-linked C-terminal telopeptide of type I collagen, procollagen type 1 N-terminal propeptide osteoprotegerin, and runt-related transcription factor 2 protein expression, was not evaluated here, but the macroscopic indicators of bone measurements used in this article can still suggest changes in bone metabolism (23)(24)(25).…”