Abstract
A rat model of secondary osteoporosis was constructed using retinoic acid as an inducer, and the genes, proteins, and bone mass of the rats were analyzed. qPCR detection of the Wnt/β-catenin and OPG/RANK/RANKL signaling pathway-related gene expression levels showed that Lactobacillus plantarum HFY15 played a positive role in regulating both pathways. HFY15 significantly increased β-catenin, Lrp5, Lrp6, Wnt10b, OPG, RANKL, and Runx2 expression and downregulated DKK1, RANK, CTSK, TRACP, and ALP expression. Enzyme-linked immunosorbent assays further confirmed the qPCR results. Tartrate-resistant acid phosphatase staining showed that HFY15 slowed retinoic acid-induced osteoclast formation. Microcomputed tomography showed that HFY15 reduced trabecular separation and increased the percent bone volume, trabecular numbers, trabecular thickness, and bone mineral density in the rats in vivo. These findings indicate that HFY15 may help prevent retinoic acid-induced secondary osteoporosis in vivo.
Highlights
Secondary osteoporosis (OP) is caused by certain diseases and treatments that interfere with bone density and cause bone loss [1]
Retinoic acid plays an important role in maintaining immune homeostasis [39] and treating Alzheimer’s disease [40]
Studies have shown that genes involved in the Wnt/β-catenin and OPG/ RANK/RANKL signaling pathways exert important effects on osteogenesis [47,48,49,50]
Summary
Secondary osteoporosis (OP) is caused by certain diseases and treatments that interfere with bone density and cause bone loss [1]. Up to 30% of postmenopausal women and 50% of men with osteoporosis may have an underlying cause [2]. People with osteoporosis generally do not experience symptoms. Osteoporosis often goes undetected for many years and is not diagnosed until a person breaks a bone. Common bone fractures related to osteoporosis include fractures of the hip, wrist, or spine. Osteoporosis occasionally causes symptoms [3]. E underlying pathogenesis of secondary osteoporosis is usually multifactorial. Treating the causes of osteoporosis can reduce the risk of fractures and prevent unnecessary treatment with anti-reabsorption drugs [4, 5]
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