Study On The Relationship Between Electroacupuncture Treatment Of LDH And The MRI Of Responsible Lesions And Its Mechanism

Objective1.Tostudytherelationshipbetweentheefficacyof electroacupuncture in the treatment of LDH and the MRI imaging of responsible lesions.2.To study the effect of electroacupuncture?EA?at Jiaji point on the expression of pCREB in degenerated intervertebral discs of rabbits,and to investigate the possible mechanism of PKA-CREB pathway involved in the regulation of AQP1,3 gene expression in endplate chondrocytes by electroacupuncture.Methods1.Clinical research60 patients were selected according to the case selection criteria.Before treatment,each patient's responsible lesions?the corresponding anatomic segments that actually caused clinical symptoms?were examined by MRI imaging of the lumbar spine.And then the MRI scores were calculated and the clinical symptoms before treatment were scored using the JOA Low Back Pain score developed by the Japanese Orthopaedic Society in 1984.Next,each patient was treated with electroacupuncture for 4 cycles.After the end of treatment,the patient's clinical symptoms were JOA scored again,and then the treatment improvement rate was calculated.Finally,statistical analysis was used to analyze the correlation between treatment improvement rate and MRI scores,in order to investigate the relationship between the efficacy of electroacupuncture in the treatment of LDH and the imaging manifestation of responsible lesions.2.Experimental research50 healthy male mature New Zealand rabbits were randomly divided into normal group,sham group,model group,model+EA group,model+EA+H89 group,10 rats in each group.The intervertebral disc degeneration model was replicated by the compression of Kirschner wire across the vertebral body.Normal group:natural feeding,without any treatment.Model group:after modeling success,without any treatment.Sham group:the same as model group,but the modeling process is not intervertebral pressure.Model+EA group:In the modeling success after the first day of acupuncture treatment,continuous treatment for 6 days for a course of treatment,each interval between 1 day treatment,a total of 4 courses of treatment.Model+EA+H89 group:PKA-CREB signal pathway inhibitor H89?10?mol/L?was injected subcutaneously on the first day after successful modeling.The normal group and the sham group at the modeling cycle,the remaining three groups after the success of the modeling of first days and twenty-eighth days,respectively 5 for L4-5disc MRI examination,and then disc tissue was harvested for ELISA,Western Blot and Real-time PCR detection.Results1.Clinical researchThe linear correlation coefficient of treatment improvement rate and MRI score was r=-0.2284,?r|<r0.05,P>0.05,indicating that there was no significant relationship between the improvement rate of treatment and MRI score.2.Experimental researchThe MRI?T₂weighted?scan showed that the degenerative intervertebral disc signal after electroacupuncture treatment was stronger than that in the model group;after the success of modeling,the expression of PKA,pCREB and AQP1,3mRNA decreased?P<0.05?;the level of expression of PKA,pCREB and AQP1,3mRNA after the intervention of electroacupuncture treatment?P<0.05?;H89 could inhibit the expression of PKA?P<0.05?,reverse the effect of electroacupuncture on up regulation of pCREB expression?P<0.05?,and decrease the expression levels of AQP1,3mRNA?P<0.05?.Conclusion1.There was no significant correlation between the efficacy of electro-acupuncture in the treatment of LDH and the MRI images of responsible lesions.2.After the lumbar intervertebral disc degeneration in model rabbits,the expression levels of AQP1 and AQP3 in the tissues decreased.Electroacupuncture could up-regulate the expression of pCREB in rabbit model of intervertebral disc degeneration through PKA-CREB pathway,and then increase the transcription of AQP1,3mRNA.Finally,the expression of AQP1,3 protein in endplate chondrocytes was increased,and the nutrient supply of cartilage endplate was increased,which delayed the degeneration of intervertebral disc and promoted the repair of degenerative intervertebral disc tissue.