Journal
BIOLOGICAL TRACE ELEMENT RESEARCH
Volume 200, Issue 8, Pages 3688-3700Publisher
SPRINGERNATURE
DOI: 10.1007/s12011-021-02967-w
Keywords
Linarin; Cadmium; Osteoporosis; Oxidative stress; Inflammation; RANK; RANKL; OPG
Funding
- Xi'an Health and Family Planning Commission 2019 Science and Technology + Action Plan -Social Development Demonstration Project
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This study found that linarin can effectively prevent bone deformities in mice exposed to cadmium, and reduce oxidative stress and inflammation by modulating the RANK/RANKL/OPG pathway.
Cadmium (Cd) contamination in the environment is a major public health concern since it has been linked to osteoporosis and other bone deformities. Linarin is a flavonoid glycoside, and it can promote osteoblastogenesis. This research aimed to investigate the potential role of linarin against Cd-exposed bone deformations in mice model. In our research, male mice were randomly allocated into four groups: control, Cd-exposed, and Cd + linarin (20 and 40mg/kg/bw, respectively). Linarin prevented body weight loss, increased serum calcium (Ca) and phosphorus (P), and bone alkaline phosphatase (BAP) levels in Cd-exposed groups. Furthermore, linarin treatment at 20 and 40mg/kg/bw significantly decreased RANK and OPG, resulting in an increase in RANKL mRNA levels and protein distribution in the bone of Cd-exposed mice. In addition, the bone of Cd-exposed mice administered with linarin showed higher TRAP, NFATc1, MMP9, and RUNX2 mRNA levels and protein distribution. Linarin significantly decreased oxidative stress in Cd-exposed mice bone by decreasing MDA, a lipid peroxidation product. Moreover, linarin protects Cd-exposed mice antioxidant enzymes by increasing bone SOD, CAT, and GPx levels. Besides, linarin suppresses alterations in the inflammatory system, i.e., NF-kappa B p65/IKK beta, by reducing NF-kappa B p65, IKK beta, IL-6, and TNF-alpha in the bone of Cd-exposed animals. This study concluded that linarin has potential to cure osteoporosis in Cd-exposed mice by reducing oxidative stress and inflammation and modulating the RANK/RANKL/OPG pathway.
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