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2024, Vol. 28 ›› Issue (28): 4498-4504

Eriodictyol accelerates glucocorticoid-induced apoptosis by promoting osteoblast autophagy

Ma Yunfeng1, Han Xiaofei2   

  1. 1Department of Osteopathy, 2Department of Rheumatology, Second Affiliated Hospital of Henan University of Chinese Medicine (Henan Province Hospital of Traditional Chinese Medicine), Zhengzhou 450002, Henan Province, China

  • Received:2023-05-21 Accepted:2023-08-16 Online:2024-10-08 Published:2023-11-27

  • Contact: Ma Yunfeng, Department of Osteopathy, Second Affiliated Hospital of Henan University of Chinese Medicine (Henan Province Hospital of Traditional Chinese Medicine), Zhengzhou 450002, Henan Province, China

  • About author:Ma Yunfeng, Master, Physician, Department of Osteopathy, Second Affiliated Hospital of Henan University of Chinese Medicine (Henan Province Hospital of Traditional Chinese Medicine), Zhengzhou 450002, Henan Province, China

  • Supported by:

    2019 Special Project for Scientific Research on Traditional Chinese Medicine of Henan Provincial Health Commission, No. 2019ZY2149 (to HXF); 2020 Special Project for Scientific Research on Traditional Chinese Medicine of Henan Provincial Health Commission, No. 20-21ZY3013 (to HXF)


Abstract: BACKGROUND: Glucocorticoid-induced osteoporosis is a common complication of systemic glucocorticoid therapy, which is mainly characterized by its inhibitory effect on osteoblasts. Eriodictyol inhibits osteoclast differentiation and osteoporosis-induced by ovariectomy. However, it is unclear whether eriodictyol regulates glucocorticoid-induced osteoblasts.
OBJECTIVE: To explore whether eriodictyol plays a role in glucocorticoid-induced osteoblast apoptosis and its potential regulatory mechanisms.
METHODS: Dexamethasone-pretreated osteoblasts MC3T3‐E1 were treated with the different concentrations (0, 0.5, 1, 2.5, 5, 10 μmol/L) of eriodictyol or 5 μmol/L 3-methyladenine, an autophagy inhibitor, and then transfected with heme oxygenase 1 overexpression vector (pcDNA-HMOX1) and empty vector (pcDNA vector). Cell proliferation and apoptosis were assessed by using cell counting kit-8 assay and flow cytometry, respectively. The activity of caspase-3 was detected with ELISA. Western blot assay was used to detect the protein expression of autophagy-related proteins LC3-II/LC3-I, p62, Atg5 and Atg12, the expression of apoptotic related proteins Bax and Bcl-2, as well as the protein expression of AMPK and p-AMPK.
RESULTS AND CONCLUSION: Low concentrations of eriodictyol were non-toxic to MC3T3-E1 cells and promoted cell proliferation, as well as increased the expression of autophagy related proteins LC3-II/LC3-I, p62, Atg5 and Atg12, decreased caspase-3 enzyme activity, inhibited Bax protein expression, promoted Bcl-2 protein expression and reduced dexamethasone-induced apoptosis in MC3T3-E1 cells in a dose-dependent manner. Moreover, eriodictyol significantly promoted heme oxygenase 1 expression in osteoblasts, whereas overexpression of heme oxygenase 1 promoted AMPK phosphorylation, activated autophagy, and inhibited dexamethasone-induced osteoblast apoptosis. While 3-methyladenine treatment counteracted the effects of heme oxygenase 1 overexpression on MC3T3-E1 cells. To conclude, low concentration of Eriodictyol is non-toxic to osteoblasts and activates AMPK signaling pathway by upregulating the expression of heme oxygenase 1, thereby promoting autophagy and inhibiting dexamethasone-induced osteoblast apoptosis. Eriodictyol has great potential for the treatment of glucocorticoid-induced osteoporosis.

Key words: eriodictyol, dexamethasone, heme oxygenase 1, MC3T3-E1 cell, the AMPK pathway


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