Platelet-Derived Biomaterials Inhibit Nicotine-Induced Intervertebral Disc Degeneration Through Regulating...

Area of Science:

• Biomedical Engineering
• Regenerative Medicine
• Spinal Health

Background:

• Adult intervertebral disc (IVD) degeneration is a complex process.
• Nicotine exposure from smoking or other sources is a potential, yet understudied, contributor to IVD pathology.
• Nicotine's known physiological effects include vascular impairment and cellular apoptosis, suggesting a role in disc degeneration.

Purpose of the Study:

• To investigate the potential of nicotine to induce intervertebral disc degeneration.
• To evaluate the dose-dependent effects of nicotine in vitro and in vivo.
• To assess the efficacy of platelet-derived biomaterials (PDB) in mitigating nicotine-induced IVD damage.

Main Methods:

• In vitro studies assessed nicotine's dose-dependent impact on chondrocytes and chondrogenic markers (Sox, Col II, aggrecan).
• In vivo studies involved subcutaneous nicotine administration in mice to observe IVD pathological changes.
• Platelet-derived biomaterials (PDB) were administered to evaluate their therapeutic potential.

Main Results:

• Nicotine significantly reduced chondrocytes and chondrogenic indicators.
• Nicotine-treated mice showed IVD structural malformation with decreased Col II and proteoglycans.
• PDB administration for 4 weeks significantly improved IVD structure and composition.
• PDB treatment restored IGF-1 signaling proteins (pIGF-1 R, pAKT, IRS-1), enhancing extracellular matrix synthesis.

Conclusions:

• Nicotine actively contributes to intervertebral disc degeneration.
• Platelet-derived biomaterials demonstrate significant reparative and regenerative capabilities.
• PDB inhibits nicotine-induced IVD degeneration by regulating the IGF-1/AKT/IRS-1 signaling axis.