Protective effects of the postbiotic Lactobacillus plantarum MD35 on bone loss in an ovariectomized mice model

Abstract

Abstract Postmenopausal osteoporosis is caused by estrogen deficiency; it impairs the homeostatic balance of the bone, resulting in bone loss owing to increased osteoclastic resorption without a corresponding increase in osteoblastic activity. Postbiotics have several pharmaceutical properties, including anti-obesity, anti-diabetic, anti-inflammatory, and anti-osteoporotic activities. However, the beneficial effects of postbiotic MD35 of Lactobacillus plantarum on bone have not been studied. In this study, we demonstrated that the postbiotic Lactobacillus plantarum MD35, isolated from young radish water kimchi influenced osteoclast differentiation in mouse bone marrow-derived macrophage (BMM) culture. In addition, it was effective in estrogen deficiency-induced bone loss in ovariectomized (OVX) mice, an animal model of postmenopausal osteoporosis. In BMM cells, postbiotic MD35 inhibited the receptor activator of nuclear factor-kappa B of NF-κB ligand (RANKL)-induced osteoclast differentiation by significantly suppressing resorption activity and downregulating the expression of RANKL-mediated osteoclast-related genes; this was achieved by attenuating the phosphorylation of extracellular signal-related kinase. In the animal model, the oral administration of postbiotic MD35 remarkably improved OVX-induced trabecular bone loss and alleviated the destruction of femoral plate growth. Therefore, postbiotic MD35 could be a potential therapeutic candidate for postmenopausal osteoporosis by suppressing osteoclastogenesis through the regulation of osteoclast-related molecular mechanisms.