Objective To explore the effect of reinforcing kidney and activating blood (RKAB) decoction on osteoporosis (OP) based on TLR4/Myd88/NF-κB signal axis. Methods Forty SD rats were randomly divided into sham operation group, model group, RKAB decoction group, and alendronate sodium group, with 10 rats in each group. Rats in the RKAB decoction group received RKAB decoction 10 mL/kg/d by gavage. Rats in the alendronate sodium group received alendronate sodium 7.35 mg/kg/d by gavage. Rats in the sham operation group and the model group received the same amount of normal saline by gavage. After 12 weeks of intervention, bone mineral density (BMD), bone mineral content (BMC), and serum Ca2+ and P levels were measured. Serum levels of TNF-α, IL 6, and IL 1β were measured with ELISA. The mRNA expression levels of TLR4, Myd88, and NF-κB in the bone tissue were detected with qRT-PCR. The protein expression levels of TLR4, Myd88, and NF-κB in the bone tissue were detected with Western blotting. The expression levels of TLR4, MyD88, and NF-κB were detected using bone transcriptomics. Results (1) BMC in the bone tissue and the levels of serum Ca2+ and P in the RKAB decoction group were higher than those in the model group (P<0.05). (2) BMD of the femur and lumbar vertebrae in the RKAB decoction group were higher than those in the model group. (3) Compared to those in the model group, the levels of IL-6, il-1β, and TNF-a in the RKAB decoction group were lower (P<0.05). (4) Compared to those in the model group, the levels of IL-6, il-1β, and TNF-a in the RKAB decoction group were lower (P<0.05). (5) Compared to those in the model group, the expression of TLR4, Myd88, and NF-κB in the RKAB decoction group decreased significantly (P<0.05), and the expression of TLR4, Myd88, and NF-κB in the RKAB decoction group decreased significantly (P<0.05). (6) The expression levels of TLR4, Myd88, and NF-κB in the RKAB decoction group were significantly lower than those in control group (P<0.05). Conclusion RKAB decoction prevents and treats osteoporosis by inhibiting TLR4/Myd88/NF-ΚB signal axis. |