Osteoporosis (OP) is a systemic bone disease with loss of bone mass and destruction of the microscopic structure. Many antiosteoporosis drugs have been used for OP therapy, but the therapeutic efficiency remains limited. Therefore, there is an urgent need to develop new drugs for antiosteoporosis treatment. Selenium (Se) is one kind of essential trace element for humans and displays pivotal roles in maintaining bone homeostasis. However, the modulation roles of Se are greatly affected by its chemical forms. Herein, Se containing protein derived from Se-enriched Spirulina platensis (Se-SP) were extracted and used for the treatment of OP in an ovariectomized mice model. The results showed that Se-SP showed enhanced potential in promoting excretion of calcium and alkaline phosphatase (ALP) expression than that of SP in MC3T3-E1 cells. Micro-CT revealed that Se-SP administration in vivo effectively alleviated bone loss as indicated by the upregulated BV, Tb.Th, Bv/TV, Tb.N, and BMD as well as the decreased Tb.Sp. Se-SP in vivo also significantly suppressed inflammatory response through restricting the expression of proinflammatory cytokines expression and upregulating the secretion of anti-inflammatory cytokines. Additionally, Se-SP effectively inhibited ovariectomy-induced osteoblast inactivation and osteoclastogenesis by upregulating BMP2, RUNX2, COL-I, OCN and OPG pression and downregulating RANKL expression. Together, these findings suggested that Se-SP was a new form of Se in therapy of human OP.

Spinal cord injury (SCI) as a serious neurological disease remains the great challenge for clinical therapy. Existing studies have confirmed that selenium (Se) supplementation could effectively decrease the risk of neurological diseases, but the mechanism is still unclear. Herein, a mouse SCI model was established, and the potential of selenomethionine (SeMet) against SCI was explored. Behavioral studies showed that SeMet administration in vivo effectively improved the motor symptoms of SCI mice. Mechanism investigation indicated that SeMet administration in vivo significantly blocked the decrease of neurons and Nissl bodies in SCI mice by inhibiting neural apoptosis. SeMet in vivo also dramatically attenuated oxidative damage of SCI mice by regulating the Nrf‐2/Keap‐1 pathway. Further studies revealed that SeMet in vivo significantly alleviated microglia activation and neuroinflammation in SCI mice, as demonstrated by the improved Iba‐1 and inflammatory factors expression, respectively. Moreover, SeMet in vivo apparently inhibited SCI‐induced cell ferroptosis of SCI mice by balancing ferroptosis‐related protein expression. Taken together, the results indicated that oxidative damage–mediated apoptosis and ferroptosis both contributed to the protective potential of SeMet against SCI, which validated the possibility that selenium‐containing agents could be promising drugs for SCI therapy.