Curcumin protects bone biomechanical properties and microarchitecture in type�2 diabetic rats with osteoporosis via the TGFβ/Smad2/3 pathway

Liang, Yujie; Zhu, Benben; Li, Shuhui; Zhai, Yun; Yang, Yi-Qiu; Bai, Zaixian; Zeng, Yuan; Li, Dawei

doi:10.3892/etm.2020.8943

Cited by 16 publications

(14 citation statements)

References 39 publications

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“…The mechanism of action in several molecular pathways is due to curcumin’s particular chemical structure, capable of having many molecular targets. The biological effects may include the inhibition of reactive oxygen species (ROS) production, playing a fundamental role, particularly for diseases related to oxidative stress and inflammation, such as DM ( 67 , 68 ). Figure 3 shows some systemic effects of curcumin.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Curcumin on Diabetes Mellitus: A Systematic Review

et al. 2021

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Diabetes mellitus (DM) is an ensemble of metabolic conditions that have reached pandemic proportions worldwide. Pathology’s multifactorial nature makes patient management, including lifelong drug therapy and lifestyle modification, extremely challenging. Currently, there is growing evidence about the effectiveness of using herbal supplements in preventing and controlling DM. Curcumin is a bioactive component found Curcuma longa, which exhibits several physiological and pharmacological properties such as antioxidant, anti-inflammatory, anticancer, neuroprotective, and anti-diabetic activities. For these reasons, our objective is to systematically review the effects of Curcuma longa or curcumin on DM. Databases such as PUBMED and EMBASE were searched, and the final selection included sixteen studies that fulfilled the inclusion criteria. The results showed that curcumin’s anti-diabetic activity might be due to its capacity to suppress oxidative stress and inflammatory process. Also, it significantly reduces fasting blood glucose, glycated hemoglobin, and body mass index. Nanocurcumin is also associated with a significant reduction in triglycerides, VLDL-c, total cholesterol, LDL-c, HDL-c, serum C reactive protein, and plasma malonaldehyde. Therefore, it can be considered in the therapeutic approach of patients with DM.

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Section: Discussionmentioning

confidence: 99%

The Effects of Curcumin on Diabetes Mellitus: A Systematic Review

et al. 2021

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“…As an antioxidant, curcumin can reduce oxidative stress, protect cells from oxidative stress damage, and play an active role in preventing and treating arthritis [ 24 ]. Another research evaluated the role of curcumin in osteogenesis, which showed that curcumin could reduce bone resorption in osteoporotic rats [ 25 ]. In the present study, we found that curcumin could inhibit inflammation response in MH7A and primary RA-FLSs by reducing TNF-α, IL-6, and IL-17 levels.…”

Section: Discussionmentioning

confidence: 99%

Curcumin alleviates rheumatoid arthritis progression through the phosphatidylinositol 3-kinase/protein kinase B pathway: an in vitro and in vivo study

Shang

Zhao

et al. 2022

Bioengineered

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Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease characterized by synovial inflammation and joint bone and cartilage destruction. Curcumin can improve joint inflammation in rats with arthritis and inhibit synovial revascularization and abnormal proliferation of fibroblasts. However, it is unclear whether curcumin affects the RA progression. The TNF-α-stimulated primary RA fibroblast-like synoviocytes (RA-FLS) and SV-40 transformed MH7A cells were used as the in vitro model of RA. A mouse model of collagen-induced arthritis (CIA) was used as the in vivo model. The effects of curcumin on cell proliferation, apoptosis, migration, invasion, and inflammatory response were assessed by colony formation, flow cytometry, wound scratch, Transwell assays, and western blotting analysis. Arthritis index scores and degree of paw swelling in mice were assessed to evaluate RA. Curcumin inhibited the TNF-α-induced proliferation, migration, invasion of MH7A and RA-FLS cells and promoted cell apoptosis. Administration with curcumin reversed the CIA-induced increase in arthritis scores, hind paw edema, and loss of appetite, while these effects were rescued by insulin-like growth factor 1, the upstream cytokine of PI3K/AKT. Moreover, curcumin suppressed the inflammatory response by reducing TNF-α, IL-6, and IL-17 secretion in CIA-stimulated mice. Curcumin has an excellent anti-RA effect in vivo and in vitro , which is exerted by inhibiting the expression of pro-inflammatory factors TNF-a, IL-6 and IL-17 and inhibiting the activation of PI3K/AKT signaling pathway. Thus, curcumin may be a promising candidate for anti-RA treatment.

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“…We found that mRNA expression of FUT8 was significantly downregulated in response to high-dose dexamethasone stimulation, along with significantly suppressed cell proliferation and osteogenic differentiation, suggesting that high-dose dexamethasone suppresses osteogenesis possibly by downregulating FUT8-mediated core fucosylation of osteogenesis-related glycoproteins. The canonical TGF-β pathway facilitates bone formation ( Baffi, Moran & Serra, 2006 ; Liang et al, 2020 ; Peters, Wang & Serra, 2017 ; Wang et al, 2013 ). Of note, FUT8-mediated core fucosylation is essential for TGF-β binding to TGFBRs ( Schachter, 2005 ; Van Staa, Leufkens & Cooper, 2002 ), and TGF-β/TGFBRs/Smads signaling is inhibited in glucocorticoid-induced osteoporosis and osteonecrosis ( Li et al, 2017 ; Tao et al, 2017 ; Xie, Hu & Shi, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of fucosyltransferase 8 reverses the inhibitory effect of high-dose dexamethasone on osteogenic response of MC3T3-E1 preosteoblasts

Lin

Kang

et al. 2021

PeerJ

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Background Core fucosylation catalyzed by FUT8 is essential for TGF-β binding to TGF-β receptors. Methods Indirect TGF-β1 binding assay was used to evaluate the ability of TGF-β1 to bind to TGFBRs, Alizarin red and alkaline phosphatase staining were used to detect osteogenic differentiation and mineralization ability , western blot and quantitative RT-PCR were used to measure the differential expression of osteogenesis-related proteins and genes. Plasmid-mediated gain-of-function study. The scale of core fucosylation modification was detected by Lectin-blot and LCA laser confocal. Results Our results showed that compared with vehicle treatment, high-dose (10−6 and 10−5 M) dexamethasone significantly inhibited cell proliferation, osteogenic differentiation, and FUT8 mRNA expression while promoting mRNA expression of adipogenesis-related genes in MC3T3-E1 cells, suggesting that downregulation of FUT8 is involved in the inhibitory effect of high-dose dexamethasone on osteogenesis. Overexpression of FUT8 significantly promoted osteogenic differentiation and activated TGF-β/Smad signaling in MC3T3-E1 cells in the presence of high-dose dexamethasone, suggesting that FUT8 reverses the inhibitory effect of high-dose dexamethasone on osteogenesis. In addition, lectin fluorescent staining and blotting showed that overexpression of FUT8 significantly reversed the inhibitory effects of high-dose dexamethasone on core fucosylation of TGFBR1 and TGFBR2. Furthermore, indirect TGF-β1 binding assay showed that overexpression of FUT8 remarkably promoted TGF-β1 binding to TGFBRs in MC3T3-E1 cells in the presence of high-dose dexamethasone. Conclusions Taken together, these results suggest that overexpression of FUT8 facilitates counteracting the inhibitory effect of dexamethasone on TGF-β signaling and osteogenesis.

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Curcumin protects bone biomechanical properties and microarchitecture in type�2 diabetic rats with osteoporosis via the TGFβ/Smad2/3 pathway

Cited by 16 publications

References 39 publications

The Effects of Curcumin on Diabetes Mellitus: A Systematic Review

The Effects of Curcumin on Diabetes Mellitus: A Systematic Review

Curcumin alleviates rheumatoid arthritis progression through the phosphatidylinositol 3-kinase/protein kinase B pathway: an in vitro and in vivo study

Overexpression of fucosyltransferase 8 reverses the inhibitory effect of high-dose dexamethasone on osteogenic response of MC3T3-E1 preosteoblasts

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