Effect Of MiR-142-3p On The Function Of Degenerative Intervertebral Disc Cartilage Endplate Cells And The Regulation Of HMGB1

Objective: Intervertebral disc degenerative disease is the reason of a series of spinal diseases.With the increasing aging of the global population,he incidence of spinal degenerative diseases is also increasing year by year,which not only harms human health but also brings heavy burden to society and economy.At present,clinical treatment methods include surgery and conservative treatment,they are mainly used to alleviate the symptoms of the disease,and can not be prevented or treated from the perspective of etiology,resulting in recurrent attacks.Cartilage endplate is not only an important tissue structure of intervertebral disc,but also an important initiating factor of degeneration.The purpose of this study is to select qualified mi RNA,to further explore the effect of mi RNA on the function of cartilage endplate cells and to clarify the relationship between mi RNA and high mobility group box-1 protein.The experimental results will provide an important theoretical basis for preventing or delay intervertebral disc cartilage endplate degeneration.Methods: In this study,Target Scan7.1 was used to predict the upstream regulation of HMGB1 mi RNA.In this study,ATDC5 cells,Primary mouse chondrocytes,were used to establish cartilage endplate cell degeneration model by low serum culture.The researchers observed the cell morphology at different stages under inverted microscope.q RT-PCR was used to detect the index of degenerative cell model,the target mi RNA was screened and the transfection efficiency was evaluated by q RT-PCR.CCK8 assay was used to detect cell proliferation,scratch test to detect cell migration,Transwell chamber test to detect cell invas ion,and flow cytometry was used to detect cell apoptosis and cell cycle.The expressions of autophagy genes P62 and Beclin1 and cell apoptosis genes Bax and Bcl-2 were detected by q RT-PCR and Western Blot methods,and the regulatory relationship between mi RNA and inflammatory factor HMGB1 was also detected.SPSS20.0 statistical software was used to analyze the statistical difference between the experimental group and the control group.Results: In the group of ATDC5-induced degenerative cells,the cells were observed to be slender at 48 h.The results showed that the expression levels of MMP13,ADAMTS5,MMP3 and Col-X were higher,while SOX9 and type II collagen were on the contrary.These results indicated that the construction of degenerative cartilage endplate cell model was completed.In the experiment of degenerative cartilage endplate cells,the expression level of mi R-142-3p was low,and the results of three experiments were stable.Low expression of mi R-142-3p inhibits cell proliferation,promotes apoptosis,changes cell cycle,and reduces cell migration and invasion.Knocking down mi R-142-3p can also inhibit the expression of Bcl-2 and promote the expression of Bax,p62 and Beclin1.Knocking down mi R-142-3p can also promote the expression of HMGB1,while overexpression of mi R-142-3p has the opposite effect.Conclusion: MiR-142-3p can change the function of degenerative cartilage endplate cells and cause intervertebral disc degeneration.HMGB1 may be a key factor in this process.These results will provide new ideas for the study of degenerative cartilage endplate.