scholarly journals Effect of Collagen Hydrolysates from Silver Carp Skin (Hypophthalmichthys molitrix) on Osteoporosis in Chronologically Aged Mice: Increasing Bone Remodeling

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1434 ◽  
Author(s):  
Ling Zhang ◽  
Siqi Zhang ◽  
Hongdong Song ◽  
Bo Li
Keyword(s):  
Body Weight ◽  
Bone Remodeling ◽  
Transforming Growth Factor ◽  
Silver Carp ◽  
Daily Intake ◽  
Transforming Growth Factor Β1 ◽  
Tartrate Resistant Acid Phosphatase ◽  
Hypophthalmichthys Molitrix ◽  
Mineral Density ◽  
Collagen Hydrolysates

Osteoporosis is a common skeletal disorder in humans and gelatin hydrolysates from mammals have been reported to improve osteoporosis. In this study, 13-month-old mice were used to evaluate the effects of collagen hydrolysates (CHs) from silver carp skin on osteoporosis. No significant differences were observed in mice body weight, spleen or thymus indices after daily intake of antioxidant collagen hydrolysates (ACH; 200 mg/kg body weight (bw) (LACH), 400 mg/kg bw (MACH), 800 mg/kg bw (HACH)), collagenase hydrolyzed collagen hydrolysates (CCH) or proline (400 mg/kg body weight) for eight weeks, respectively. ACH tended to improve bone mineral density, increase bone hydroxyproline content, enhance alkaline phosphatase (ALP) level and reduce tartrate-resistant acid phosphatase 5b (TRAP-5b) activity in serum, with significant differences observed between the MACH and model groups (p < 0.05). ACH exerted a better effect on osteoporosis than CCH at the identical dose, whereas proline had no significant effect on repairing osteoporosis compared to the model group. Western blotting results demonstrated that CHs mainly increased bone remodeling by stimulating the transforming growth factor β1 (TGF-β1)/Smad signaling pathway and improving the interaction between collagen and α2β1 integrin. The results indicated that CHs from fish could be applied to alleviate osteoporosis or treat bone loss.

scholarly journals Violations of cell-molecular mechanisms of bone remodeling under influence of glucocorticoids

2018 ◽  
Vol 9 (1) ◽  
pp. 124-129
Author(s):  
S. B. Pavlov ◽  
N. M. Babenko ◽  
M. V. Kumetchko ◽  
O. B. Litvinova
Keyword(s):  
Bone Tissue ◽  
Bone Remodeling ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Tissue Remodeling ◽  
Transforming Growth Factor Β1 ◽  
Control Group ◽  
Interleukin 17 ◽  
Mineral Density ◽  
Bone Tissue Remodeling

The fact is disturbance of the processes of bone tissue remodeling leads to a change in the balance between synthesis and resorption of bone and the development of osteoporosis. The most common cause of secondary osteoporosis is the use of glucocorticoid therapy. The aim of this study is to investigate the cellular-molecular mechanisms of disturbance of the processes of bone remodeling regulation, reflected by hormones and intercellular mediators (for example parathyroid hormone, calcitonin, RANKL, osteoprotegerin, P-selectin, interleukin-17, transforming growth factor-β1, adiponectin and visfatin) on the background experimental glucocorticoid osteoporosis. The experimental study carried out in two groups of white female rats. Disturbance of bone tissue remodeling was verified by histological examination of the femoral head, vertebrae of the thoracic and lumbar spine of rats and the measurement of bone density. The study of the levels of hormones and intercellular mediators in the blood serum of animals was carried out by the method of enzyme immunoassay. The bone mineral density of the experimental group was reduced compared to the bone mineral density of the control group. The study of the histostructure of the femoral head and vertebrae in rats of the experimental group in comparison with the animals of the control group revealed changes in the structural organization of bone tissue, confirmed by histomorphometry, indicating inhibition of the processes of osteosynthesis. The article analyzes the nature of the involvement of hormones and cytokines in pathogenetic mechanisms of development of bone tissue disorders. The levels of cytokines RANKL, osteoprotegerin, interleukin-17 and calcitonin in the blood serum of animals of the group with the violation of bone tissue remodeling by glucocorticoids were higher than in intact animals. Serum levels of P-selectin, parathyroid hormone, transforming growth factor-β1, adiponectin and visfatin were lower than similar levels in animals from the control group. The use of glucocorticoids increases the expression of RANKL and inhibits the synthesis of osteoprotegerin, resulting in stimulation of bone resorption. The effect of glucocorticoids in the experimental model is realized by changing the production of the studied hormones, cytokines and adhesion molecules. These changes stimulate the apoptosis of osteoblasts and inhibit their proliferation and differentiation, which is another mechanism of bone loss. Correlations found during the study reflect the relationship in the system of regulation of bone tissue remodeling under the influence of glucocorticoids. A complex system for regulating bone remodeling, which includes many regulatory pathways and their interactions, requires further study.

Emerging Role of Extracellular Vesicles in Bone Remodeling

2018 ◽  
Vol 97 (8) ◽  
pp. 859-868 ◽  
Author(s):  
M. Liu ◽  
Y. Sun ◽  
Q. Zhang
Keyword(s):  
Bone Remodeling ◽  
Extracellular Vesicles ◽  
Transforming Growth Factor ◽  
Tooth Development ◽  
Osteoclast Differentiation ◽  
Nuclear Factor Κb ◽  
Transforming Growth Factor Β1 ◽  
Bone Diseases ◽  
Bioactive Molecules

Extracellular vesicles (EVs), as nanometer-scale particles, include exosomes, microvesicles, and apoptotic bodies. EVs are released by most cell types, such as bone marrow stem cells, osteoblasts, osteoclasts, and immune cells. In bone-remodeling microenvironments, EVs deliver specific proteins (e.g., tenascin C and Sema4D), microRNAs (e.g., miR-214-3p, miR-183-5p, and miR-196a), and other growth factors (e.g., bone morphogenetic protein 1 to 7 and transforming growth factor β1) to osteoblasts and regulate bone formation. In addition, EVs can deliver cytokines, such as RANK (receptor activator of nuclear factor κB) and RANKL (RANK ligand), and microRNAs, such as miR-218 and miR-148a, to modulate osteoclast differentiation during bone resorption. EVs also transfer bioactive molecules and have targeted therapies in bone-related diseases. Moreover, bioactive molecules in EVs are biomarkers in bone-related diseases. We highlight the emerging role of EVs in bone remodeling during physiologic and pathologic conditions and summarize the role of EVs in tooth development and regeneration. At the end of this review, we discuss the challenges of EV application in the treatment of bone diseases.

The effect of collagen hydrolysates from silver carp (Hypophthalmichthys molitrix) skin on UV-induced photoaging in mice: molecular weight affects skin repair

2017 ◽  
Vol 8 (4) ◽  
pp. 1538-1546 ◽  
Author(s):  
Hongdong Song ◽  
Mengfei Meng ◽  
Xiaofeng Cheng ◽  
Bo Li ◽  
Chengtao Wang
Keyword(s):  
Molecular Weight ◽  
Silver Carp ◽  
Hypophthalmichthys Molitrix ◽  
Beneficial Effects ◽  
Skin Repair ◽  
Collagen Hydrolysates

LMCH exerted stronger beneficial effects on photoaging skin than HMCH and gelatin.

scholarly journals Effect of Intermittent Fasting on Glucose Homeostasis and Bone Remodeling in Glucocorticoid-Induced Osteoporosis Rat Model

2021 ◽  
Vol 28 (4) ◽  
pp. 307-316
Author(s):  
Majed G. Alrowaili ◽  
Abdelaziz M. Hussein ◽  
Elsayed A. Eid ◽  
Mohamed S. Serria ◽  
Hussein Abdellatif ◽  
...  
Keyword(s):  
Bone Remodeling ◽  
Bone Mineral ◽  
Serum Levels ◽  
Male Rats ◽  
Control Group ◽  
Intermittent Fasting ◽  
Tartrate Resistant Acid Phosphatase ◽  
Type I ◽  
Mineral Density ◽  
Trap 5B

Background: The present study examined the effect of intermittent fasting (IF) on bone mineral content (BMC) and bone mineral density (BMD) and the markers of bone remodeling in a glucocorticoid-induced osteoporosis (GIO) rat model.Methods: Forty male rats were allocated to 4 groups (N=10 per group): control group of normal rats; control+IF group (normal rats subjected to IF for 16-18 hr daily for 90 days); dexamethasone (DEX) group: (DEX [0.5 mg i.p.] for 90 days); and DEX+IF group (DEX and IF for 90 days). By the end of the experiment, BMD and BMC in the right tibia were measured. Serum levels of the following were measured: glucose; insulin; triglycerides (TGs); total cholesterol; parathyroid hormone (PTH); osteoprotegerin (OPG); receptor activator of nuclear factor-κB (RANK); bone-resorbing cytokines, including bone deoxypyridinoline (DPD), N-terminal telopeptide of collagen type I (NTX-1), and tartrate-resistant acid phosphatase 5b (TRAP-5b); and bone-forming cytokines, including alkaline phosphatase (ALP) and osteocalcin (OC).Results: DEX administration for 90 days resulted in significantly increased serum levels of glucose, insulin, TGs, cholesterol, PTH, OPG, DPD, NTX-1, and TRAP-5b and significantly decreased BMD, BMC, and serum levels of RANK, OC, and ALP (all P<0.05). IF for 90 days significantly improved all these parameters (all P<0.05).Conclusions: IF corrected GIO in rats by inhibiting osteoclastogenesis and PTH secretion and stimulating osteoblast activity.

scholarly journals Interspecies Comparison of Alveolar Bone Biology, Part I: Morphology and Physiology of Pristine Bone

2020 ◽  
pp. 238008442093697
Author(s):  
I. Pilawski ◽  
U.S. Tulu ◽  
P. Ticha ◽  
P. Schüpbach ◽  
H. Traxler ◽  
...  
Keyword(s):  
Animal Models ◽  
Bone Remodeling ◽  
Alveolar Bone ◽  
State Of The Art ◽  
Tartrate Resistant Acid Phosphatase ◽  
Knowledge Gap ◽  
Bone Biology ◽  
Mineral Density ◽  
Surgical Interventions

Introduction: Few interspecies comparisons of alveolar bone have been documented, and this knowledge gap raises questions about which animal models most accurately represent human dental conditions or responses to surgical interventions. Objectives: The objective of this study was to employ state-of-the-art quantitative metrics to directly assess and compare the structural and functional characteristics of alveolar bone among humans, mini pigs, rats, and mice. Methods: The same anatomic location (i.e., the posterior maxillae) was analyzed in all species via micro–computed tomographic imaging, followed by quantitative analyses, coupled with histology and immunohistochemistry. Bone remodeling was evaluated with alkaline phosphatase activity and tartrate-resistant acid phosphatase staining to identify osteoblast and osteoclast activities. In vivo fluorochrome labeling was used as a means to assess mineral apposition rates. Results: Collectively, these analyses demonstrated that bone volume differed among the species, while bone mineral density was equal. All species showed a similar density of alveolar osteocytes, with a highly conserved pattern of collagen organization. Collagen maturation was equal among mouse, rat, and mini pig. Bone remodeling was a shared feature among the species, with morphologically indistinguishable hemiosteonal appearances, osteocytic perilacunar remodeling, and similar mineral apposition rates in alveolar bone. Conclusions: Our analyses demonstrated equivalencies among the 4 species in a plurality of the biological features of alveolar bone. Despite contradictory results from older studies, we found no evidence for the superiority of pig models over rodent models in representing human bone biology. Knowledge Transfer Statement: Animal models are extensively used to evaluate bone tissue engineering strategies, yet there are few state-of-the-art studies that rigorously compare and quantify the factors influencing selection of a given animal model. Consequently, there is an urgent need to assess preclinical animal models for their predictive value to dental research. Our article addresses this knowledge gap and, in doing so, provides a foundation for more effective standardization among animal models commonly used in dentistry.

Chronic treatment with angiotensin AT1 receptor antagonists reduced serum but not bone TGF-β1 levels in ovariectomized rats

2009 ◽  
Vol 87 (1) ◽  
pp. 51-55 ◽  
Author(s):  
Yong-Qi Li ◽  
Hui Ji ◽  
Yang Shen ◽  
Li-Ju Ding ◽  
Pei Zhuang ◽  
...  
Keyword(s):  
Bone Loss ◽  
Postmenopausal Osteoporosis ◽  
Chronic Treatment ◽  
Transforming Growth Factor ◽  
Ovariectomized Rats ◽  
Tartrate Resistant Acid Phosphatase ◽  
Mineral Density ◽  
Receptor Antagonists ◽  
Ovx Rats ◽  
At1 Receptor Antagonists

Approximately 50% of hypertensive patients are postmenopausal women; therefore, any antihypertensive therapy must not adversely affect bone loss in this population. Recently, however, concern has been raised that use of angiotensin AT1 receptor antagonists may increase the tendency to develop postmenopausal osteoporosis by decreasing transforming growth factor-β1 (TGF-β1), which has been implicated in bone mass maintenance. In the present study, we selected telmisartan and valsartan as representatives of angiotensin AT1 receptor antagonists and used ovariectomized (OVX) rats as a model of human postmenopausal osteoporosis. After 3 months treatment with telmisartan (5 mg/kg daily) or valsartan (10 mg/kg daily), OVX rats showed no signs of adverse effects on bone mineral density of the lumbar vertebrae (L1–L5) or the total femur, nor did treatment affect serum levels of osteocalcin and osteoclast-derived tartrate-resistant acid phosphatase (TRACP-5b). Bone TGF-β1 content remained unchanged, although treatment with telmisartan and valsartan significantly reduced serum TGF-β1 levels (p < 0.05). In conclusion, chronic treatment with angiotensin AT1 receptor antagonists reduced serum but not bone TGF-β1 levels and did not accelerate ovariectomy-induced bone loss in rats.

Changes in the immunohistochemical localisation of fibroblast growth factor-2, transforming growth factor-β1 and thrombospondin-1 are associated with early angiogenic events in the hyperplastic rat thyroid

1996 ◽  
Vol 148 (3) ◽  
pp. 485-499 ◽  
Author(s):  
V A Patel ◽  
D J Hill ◽  
M C Eggo ◽  
M C Sheppard ◽  
G P Becks ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Body Weight ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Follicular Cells ◽  
Rat Thyroid

Abstract Administration of a goitrogen (methimazole) and a low iodine diet to rats over a two-week period resulted in hypothyroidism and thyroid hyperplasia compared with controls (control: total serum thyroxine (T4) 66 ± 4 nmol/l, thyroid weight 5±1 mg/100 g body weight; experimental: T4 undetectable, thyroid weight 27 ± 4 mg/100 g body weight after 2 weeks of treatment; mean ± s.d., n=10). Immunohistochemistry carried out using a specific endothelial cell marker, CD31, and morphometric analysis (point counting of immunopositive cells) revealed that the progression of goitre in the rat thyroid is accompanied by an increase in capillary endothelial cell growth (neovascularisation). Fibroblast growth factor-2 (FGF-2) immunohistochemistry revealed widespread staining for the protein in the follicular cells of control glands. Less intense staining was found in the stroma and follicular cell nuclei. During hyperplasia and subsequent neovascularisation there was a progressive increase in the FGF-2 immunoreactivity at all locations during the two-week treatment period. Thrombospondin-1 (TSP1) immunoreactivity in the control rat thyroid was found in the stroma and in the endothelial cells, while weak follicular cell staining was also present. In the goitrous rat thyroid the TSP1 immunoreactivity was present after 1 week of treatment in the endothelial cells and most follicular cells, whilst stromal localisation was weak. After week 2 of treatment the endothelial cell and stromal localisation was no longer apparent, although a follicular localisation was still present. Transforming growth factor-β1 (TGFβ1) immunoreactivity was present in the cytoplasm of a minority of the follicular cells in control rat thyroids, while their nuclei were unstained. In the goitrous rat thyroid an increased intensity of staining for TGFβ1 was seen in all follicular cells, many of which now also demonstrated immunopositive nuclei, within one week of goitrogen administration. These results show that in the hyperplastic thyroid increases in FGF-2 and TGFβ1, and decreases in TSP1, accompany angiogenesis. These factors may interact in an autocrine/paracrine relationship to stimulate the neovascularisation that occurs during goitre formation. Journal of Endocrinology (1996) 148, 485–499

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