Lycium barbarum polysaccharide protects BMSCs against cadmium-induced suppression of osteogenic differentiation by modulating autophagy

Cadmium (Cd), a heavy metal pollutant that accumulates in organisms, is osteotoxic and contributing to the development of osteoporosis. Lycium barbarum polysaccharide (LBP), a polysaccharide obtained from the Chinese medicinal plant Lycium barbarum, exhibits protective effects against oxidative stre...

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Main Authors: Liang-xu Wei, Yan Cui, Yan-lan Lv, Qian-yun Ye, Jian-bing Chen, Xiao-yao Zhan, Zi-jun Zhu, Xiao-feng Zhu, Bei Zhou
Format: Article
Language:English
Published: Elsevier 2025-04-01
Series:Ecotoxicology and Environmental Safety
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Online Access:http://www.sciencedirect.com/science/article/pii/S0147651325004841
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Summary:Cadmium (Cd), a heavy metal pollutant that accumulates in organisms, is osteotoxic and contributing to the development of osteoporosis. Lycium barbarum polysaccharide (LBP), a polysaccharide obtained from the Chinese medicinal plant Lycium barbarum, exhibits protective effects against oxidative stress and cellular damage. However, it is unclear whether LBP can effectively inhibit Cd-induced osteotoxicity. This study investigated whether LBP alleviates Cd-induced osteogenic suppression in bone marrow mesenchymal stem cells (BMSCs) via autophagy modulation. Cell viability, osteogenic markers (ALP, BMP2, COL1, RUNX2), and mineralization were assessed using CCK-8, qPCR, Western blot, and alizarin red staining. Autophagy flux was evaluated via GFP-mCherry-LC3B transfection and protein markers (LC3-II, P62, BECN). We confirmed that Cd inhibited the formation of cellular autophagosomes while adversely affecting BMSCs. However, LBP mitigated the Cd-induced osteogenic inhibitory effect by stimulating the autophagy processes and facilitating the formation of autophagosomes and autolysosomes. In conclusion, LBP is a potential bone-enhancing agent that can improve cell viability and osteogenic differentiation while mitigating the detrimental effects of Cd on BMSCs through the activation of autophagy.
ISSN:0147-6513