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. 2023 Nov 15;18(1):867.
doi: 10.1186/s13018-023-04276-5.

Association between dietary selenium intake and the prevalence of osteoporosis and its role in the treatment of glucocorticoid-induced osteoporosis

Yi Luo #  1 , Yaolin Xiang #  2 , Banghua Lu  1 , Xiaoyan Tan  1 , Yanqiong Li  1 , HuiHui Mao  1 , Qin Huang  3
Affiliations

Association between dietary selenium intake and the prevalence of osteoporosis and its role in the treatment of glucocorticoid-induced osteoporosis

Yi Luo et al. J Orthop Surg Res. .

Erratum in

Abstract

Background: Long-term glucocorticoid therapy may lead to osteoporosis (OP). Selenium (Se) is an essential microelement for human health and bone health. This study evaluated the association between dietary Se intake and the prevalence of OP and further explored the potential therapeutic effect of Se on glucocorticoid-induced OP (GIOP) in vivo and in vitro.

Methods: Data were collected from a population-based cross-sectional study conducted in our hospital. OP is diagnosed based on bone mineral density (BMD) measurements using compact radiographic absorptiometry. Dietary Se intake was assessed using a semi-quantitative food frequency questionnaire. The association between dietary Se intake and OP prevalence was analyzed by multivariable logistic regression. In animal experiments, male Sprague-Dawley rats were intramuscularly injected with dexamethasone (1 mg/kg) daily to induce GIOP, while different doses of Se were supplemented in rat drinking water for 60 d. BMD and biomechanical parameters of rat femur were measured. The histopathological changes of the femur were observed by HE staining, the number of osteoclasts was observed by TRAP staining, and OCN positive expression was detected by immunohistochemical staining. OPG, RANKL, Runx2, and BMP2 in rat femur were detected by Western blot. Bone turnover markers and oxidative stress markers were measured using commercial kits. MC3T3-E1 cells were induced to osteogenic differentiation, stimulated with DXM (100 μM), and/or treated with Se at different doses. Cell proliferation and apoptosis were assessed by CCK-8 and flow cytometry. ALP activity was detected by ALP staining and cell mineralization was observed by alizarin red staining.

Results: Participants with lower dietary Se intake had higher OP prevalence. Se supplementation improved BMD, biomechanical parameters, and histopathological changes of the femur in GIOP rats. Se supplementation also suppressed DXM-induced changes in bone turnover- and oxidative stress-related markers. Under DXM conditions, Se treatment induced MC3T3-E1 cell proliferation, ALP activity, and mineralization.

Conclusion: Lower Dietary Se intake is associated with OP prevalence. Moreover, Se takes a position in bone protection and anti-oxidative stress in GIOP models. Therefore, Se may be a complementary potential treatment for GIOP.

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Conflict of interest statement

The authors have no conflicts of interest to declare.

Figures

Fig. 1
Fig. 1
Effect of Se supplementation on BMD and histopathological changes of femur in GIOP rats. A BMD was measured by DEXA; B–D Biomechanical parameters of femur were determined by three-point bending test; E–F Histopathological changes of femur were observed by HE staining and TRAP staining; G Immunohistochemical detection of OCN positive expression. Values are expressed as mean ± SD. n = 6; * vs. Sham, P < 0.05; # vs. Model, P < 0.05
Fig. 2
Fig. 2
Effect of Se supplementation on bone metabolism in GIOP rats. A RANKL/OPG in femur tissue was detected by Western blot; B–C Serum OCN and CTX levels; D Runx2 and BMP2 in femur were detected by Western blot. Values are expressed as mean ± SD. n = 6; * vs. Sham, P < 0.05; # vs. Model, P < 0.05
Fig. 3
Fig. 3
Effect of Se supplementation on serum markers of oxidative stress in GIOP rats. A–C Levels of serum oxidative stress markers (MDA, GSH and SOD) in GIOP rats. Values are expressed as mean ± SD. n = 6; * vs. Sham, P < 0.05; # vs. Model, P < 0.05
Fig. 4
Fig. 4
Effects of Se treatment on MC3T3-E1 cell function and oxidative stress. A MC3T3-E1 cell proliferation was detected by CCK-8; B MC3T3-E1 cell apoptosis was detected by flow cytometry; C–D Activity of antioxidant enzymes (SOD and GSH) in MC3T3-E1 cells. Values are expressed as mean ± SD; N = 3; * vs. Control, P < 0.05; # vs. DXM, P < 0.05
Fig. 5
Fig. 5
Effect of Se treatment on ALP activity and mineralization in MC3T3-E1 cells. A ALP activity was analyzed by ALP staining; B Formation of mineralized nodules was observed by Alizarin red staining; C Runx2 and BMP2 in MC3T3-E1 cells were detected by Western blot. Values are expressed as mean ± SD; N = 3; * vs. Control, P < 0.05; # vs. DXM, P < 0.05
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