An Animal Model Of Intervertebral Disc Degeneration Induced By TNF-α

Background: Lumbar disc herniation is a common disease of bone to low back pain asthe main clinical manifestations, seriously affecting the quality of life of patients.Proinflammatory cytokines play an important role in Intervertebral disc degeneration(IDD),Tumour necrosis factor-alpha (TNF-α) has been demonstrated to be expressedabnormally in IDD.Objective:To construct an animal model of intervertebral disc degeneration by the useof TNF-αand research the influence of TNF-α on nucleus pulposus tissue.Methods:30healthy New Zealand white rabbits were selected as experimental animals.The lumbar intervertebral discs were exposured by anterior approach.The TNF-α wasinjected into L3/4、L4/5for experimental group, while PBS was injected to L5/6forcontrol group,L2/3was used as a blank group.X-ray irradiation, MRI and histologicalobservation for handled discs at4,8,12weeks after injection were measuredrespectively.Result:The expression of Ⅰcollagens and bax and cell apoptosis were significantlyincreased in experimental group,when compared to the blank group and controlgroup(P<0.05).The intervertebral disc height,expression of Ⅱ collagens and bcl-2were significantly decreased in experimental group when compared to the blank groupand control group(P<0.05).The intensity of T2signal in the experimental group wasdeclined with the time going.MRI assessment showed significant differences betweenthe experimental group and the blank group from the fourth week on (P<0.05).Theintervertebral disc height,MRI,expression of Ⅰ,Ⅱcollagens,bax, bcl-2and cellapoptosis did not show a significant difference in control group when compared to theblank group(P>0.05).Conclusion:1.TNF-α can influence the expression of Ⅰ,Ⅱ collagens and induceapoptosis of nucleus pulposus cells.TNF-α can induce the degeneration of intervertebraldisc.2.The microsyringe puncture can not induce the degeneration of intervertebral disc.3.Bcl-2, Bax play an important regulatory role in TNF-alpha-induced degenerativeprocess.