Table 1 Mechanisms of action mediated by the SNS in osteoporosis
Experimental model | Bone cell lineage | Key Factors | Intervention | Actions and their mechanisms | Ref. |
|---|---|---|---|---|---|
In vivo: SD rats | OB, OC | NE | Chemical sympathectomy; guanethidine (40 mg/kg/day, i.p.) for 5 weeks | NE promotes osteoclastogenesis by activating β-AR, upregulating RANKL expression. NE also suppresses osteogenesis by inhibiting α-AR, decreasing OPG and osteocalcin expression. | |
In vivo: OVX mice; in vitro: BMSCs | BMSCs, OB, OC | ACh | In vivo: NRTN injections (0.5, 1, 2 mg/kg, i.v.) twice weekly for 4 weeks; in vitro: NRTN added to osteogenic medium | NRTN directly promotes the osteoblastic differentiation of BMSCs without affecting their proliferation or osteoclast differentiation. | |
In vivo: SD rats; in vitro: BMSCs | BMSCs, OB, OC | NPY | In vivo: MLT; NPY1R inhibitor (20 μg/rat/q2d); in vitro: MLT (2 mmol/L) ± NPY1R inhibitor (0.1 mmol/L) in MSC medium | MLT activates NPY/NPY1R signaling, promoting MSC proliferation, migration, and osteogenic differentiation. | |
In vivo: OVX mice; in vitro: Bone marrow cells | OB, OC | NPY | In vivo: Y2 receptor antagonist i.p.; in vitro: Y2 receptor antagonist in culture medium | Y2 receptor antagonist suppresses hypothalamic Y2 receptors, leading to the centrally mediated promotion of osteogenesis and the inhibition of osteoclastogenesis. | |
In vivo: Adrb2−/− (β2-AR KO), Dbh−/− (DBH KO), ob/ob (leptin-def.), Cart−/− (CART KO) mice; in vitro: OB, OC, BMCs | OB, OC | Leptin | In vivo: ICV; OVX; in vitro: ISO; PKA inhibitor; ATF4 mutant transfection | Sympathetic activation via β2-AR inhibits osteoclast differentiation. Leptin suppresses osteogenesis via the hypothalamus-sympathetic nerve axis. CART peptide antagonizes bone resorption. | |
In vivo: naturally aged SD rats | OB, OC | Leptin | Qing’e Formula extract | Extract enhances leptin signaling, ameliorates the imbalance between osteogenesis and bone resorption, and increases BMD. |
