Lycium barbarum polysaccharide protects against osteonecrosis of femoral head via regulating Runx2 expression

•LBP enhanced osteoblast differentiation of BMSCs under hypoxia condition.•LBP treatment enhanced Runx2 and ALP expression in BMSCs.•LBP protects against ONFH via regulating Runx2 expression, which could be utilized to treat patients suffering ONFH. Osteonecrosis of femoral head (ONFH) is a patholog...

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Published in:Injury 2022-04, Vol.53 (4), p.1361-1367
Main Authors: Song, Qiang, Yong, Hai-Ming, Yang, LV-Lin, Liang, Yu-Qi, Liu, Ze-Xin, Niu, Dong-Sheng, Bai, Zhi-Gang
Format: Article
Language:English
Subjects:
BMSC
Bone mesenchymal-derived stem cells
Lycium barbarum polysaccharide
Osteoblast differentiation
Osteonecrosis of femoral head
Runx2
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Summary:•LBP enhanced osteoblast differentiation of BMSCs under hypoxia condition.•LBP treatment enhanced Runx2 and ALP expression in BMSCs.•LBP protects against ONFH via regulating Runx2 expression, which could be utilized to treat patients suffering ONFH. Osteonecrosis of femoral head (ONFH) is a pathological state caused by lack of blood supply in femoral head. This study aimed to explore the function of Lycium barbarum polysaccharide (LBP), an antioxidant agent extracted from L. barbarum, on ONFH. Osteonecrosis rat model was generated using lipopolysaccharide (LPS) and methylprednisolone followed by examination of body weight, blood glucose, morphology, and BMSC osteoblast differentiation. The effect and underlying mechanism of LBP on the proliferation, apoptosis, and osteoblast differentiation of BMSC were determined with or without LPS or hypoxia treatment using CCK-8. Alizarin Red S staining, flow cytometry, and western blot, respectively. LBP could protect against glucocorticoid-induced ONFH in rats, resulting in improved sparse trabecular bone, empty lacunae and bone cell coagulation. Moreover, LBP promoted the proliferation and osteoblast differentiation of bone mesenchymal-derived stem cells (BMSCs) in a dose-dependent manner. Furthermore, LBP enhanced osteoblast differentiation of BMSCs under hypoxia condition. Mechanistically, we found that LBP treatment enhanced Runx2 and ALP expression in BMSCs. LBP restored the expression of Runx2 and ALP under hypoxia, suggesting that LBP might be involved in regulating Runx2/ALP expression and contributed to osteoblast differentiation. Knockdown of Runx2 significantly inhibited BMSCs proliferation, while LBP treatment did not rescue the osteoblast differentiation ability of BMSCs with Runx2 knockdown. Our findings suggested that LBP protects against ONFH via regulating Runx2 expression, which could be utilized to treat patients suffering ONFH.
ISSN:0020-1383
1879-0267
DOI:10.1016/j.injury.2021.12.056