尼古丁对大鼠BMSCs修复软骨缺损的干预作用研究

Objective To confirm nicotine's adverse effect on the chondrogenic repair of BMSCs in rat articular cartilage defects through the suppression of Sox9. Methods Whole bone marrow adherence method was used to expand BMSCs from primary passage to third passage. Forty 12-weeks Wistar rats (male: female =1:1) were used to create cartilage defect model. The rats were randomized into 4 groups: Non-treated group: no treatment in articular cartilage defect model; Alginate group: repair the cartilage defect with alginate gel only; BMSCs group: repair the cartilage defect with alginate gel and BMSCs; Nicotine group: nicotine 2.0 mg/kgo d was injected every day after repairing the cartilage defect with alginate gel and BMSCs. Rats were sacrificed under ether anesthesia 3 month after operation and distal part of the femur was examined. Results Nicotine could repress the cartilage repair, gene expression of Col2A1, Aggrecan and Sox9 regenerated cartilage tissues were lower. Conclusion BMSCs with Alginate gel transplantation was an effective method to repair articular cartilage defects. Nicotine has an adverse effect on repair outcome through suppressing the expression of Sox9.)