Study on the Repair Mechanism of Regulatory T Cells Transforming Growth Factor β1 Induced by to Inhibit the Absorption of flammatory Bone Defect

YANG Junlong; LIANG Huiquan; OU Zefeng; LIN Jinhao; BAI Rongfei; ZHANG Zijie; WANG Guoliang

doi:10.14033/j.cnki.cfmr.2025.06.002

Abstract：Objective:To analyze the repair mechanism of Transforming Growth Factor-betal(TGF-β1)induced by regulatory T cells to inhibiting the absorption of inflammatory bone defect.Method:A total of 25 healthy New Zealand white rabbits were selected to construct a high-specificity animal model of femoral condylar bone defect of knee joint.Finally,20 animal models were successfully constructed and randomly divided into group A and group B with 10 rabbits each,and 10 healthy New Zealand white rabbits were included as a blank control group.The group A were injected subcutaneously with 5 ng/mL TGF-β1 solution(2 days/time)on both knee joints,the blank control group were injected with equal volume of normal saline,group B were not injected,and rabbits in the three groups were routinely fed for 14 days.The levels of serum inflammatory factors and the expressions of microbial DNA methyltransferase 1(DNMT1),TGF-β1,RUNt-related transcription factor 2(Runx2)and osteopontin(OPN)in femoral condylar bone defect of knee joint of rabbits were compared among the three groups.Result:The serum levels of tumor necrosis factor-α(TNF-α),interleukin-6(IL-6)and C-reactive protein(CRP)in group B were higher than those in group A and blank control group,and the differences were statistically significant(P<0.05).There was no significant difference in serum TNF-α,IL-6 and CRP levels between group A and blank control group(P>0.05).The expressions of DNMT1,TGF-β1,Runx2 and OPN in femoral condylar bone defect tissue of knee joint of rabbits in group B were lower than those in group A and blank control group,and the differences were statistically significant(P<0.05).Conclusion:TGF-β1 can alleviate the inflammatory response of high specificity rabbit knee joint femoral condylar bone defects and promote osteogenic differentiation.