The Model Of Cartilage Endplate Degeneration In Rats Was Established,and The Influence Of MiRNA/HMGB1 On Cartilage Endplate Degeneration And Its Mechanism Were Explored

OBJECTIVE The mechanisms of intervertebral disc degeneration are complex and diverse and still unknown.Studying the specific mechanisms of disc degeneration can provide theoretical support for finding treatments to delay disc degeneration,which can not only relieve patients’ pain but also improve the social burden caused by related diseases.The cartilage endplate is one of the important structures of the intervertebral disc,and its degeneration is an important cause of disc degeneration.In this experiment,we constructed a rat cartilage endplate degeneration model,aiming to investigate the mechanism of mi R-142-3p and HMGB1 on cartilage endplate degeneration in an early complex in vivo model.METHODS Forty SD rats were selected and divided into Sham group,Model group,mi R-NC group,mi R-142-3p mimics group,mi R-142-3p inhibitor group,and mi R-142-3p mimics+HMGB1 overexpression group.The target intervertebral disc segments of rats were punctured using the puncture method.The corresponding groups were injected with saline,mi R-NC,mimics,inhibitor and HMGB1 lentivirus in the tail vein once a week for 2 times after 2 weeks of modeling.6 weeks later,the rats were executed and cartilage endplate tissue was removed.HE staining was performed to observe the degeneration of cartilage endplates.TUNEL staining was performed to observe AFoptosis in different groups of cartilage endplates.q RT-PCR assay was performed to detect the expression of mi R-142-3p in cartilage endplates.western blot assay was performed to detect the expression of HMGB1,bcl-2,bax,caspase-3,cleaved-Caspase-3 in cartilage endplates.cleaved-Caspase-3 expression in cartilage endplate tissue.RESULTS Compared with the Sham group,the Model group showed a large number of fissures and infiltrated by a large number of inflammatory cells in the tissue part,as well as more fibrous-like cells,and the degeneration was obvious,indicating that the rat cartilage endplate tissue degeneration model was successfully modeled.Knockdown of mi R-142-3p and overexpression of HMGB1 promoted cartilage endplate degeneration,and overexpression of mi R-142-3p inhibited degeneration.AFoptosis-positive cells were significantly increased in rat degenerated cartilage endplate tissue.Inhibition of mi R-142-3p and HMGB1 promoted AFoptosis of cartilage endplate cells,and overexpression of mi R-142-3p inhibited AFoptosis.The expression of mi R-142-3p and bcl-2 was significantly decreased and the expression of HMGB1,bax,and cleaved-Caspase-3 was significantly increased in degenerated cartilage in rats that could not be tissues.Inhibition of mi R-142-3p promoted the expression of bax,cleaved-Caspase-3 and inhibited the expression of bcl-2 in degenerating cartilage endplate tissue.Promoting HMGB1 expression promoted bax,cleaved-Caspase-3 expression and inhibited bcl-2 expression in degenerated cartilage endplate tissues.CONCLUSIONS The expression level of mi R-142-3p was significantly reduced and that of HMGB1 was significantly increased in rat cartilage endplate tissues.Meanwhile,low expression of mi R-142-3p could promote cell dropout of rat cartilage endplates through upregulating HMGB1 expression and promote the expression of bax and cleaved-Caspase-3 and inhibit the expression of bcl-2,which led to the degeneration of rat cartilage endplates.