The Intervention Of Baoshen' Recipe On JNK-MAPK Pathway In The Kidney Tissue Of Diabetic Mice

Diabetic nephropathy is one of diabetic whole body microangiopathy complications.There is an upward trend in the incidence in our country,and it has become the second cause of end-stage renal disease after all kinds of glomerulonephritis.So we should explore deeply the pathogenesis of diabetes and diabetic nephropathy,and actively search and develop new treatment and new drugs to intervent diabetic nephropathy at earlier stage.Objective: This research use STZ(Streptozotocin,STZ)to induce diabetic nephropathy in mice model and give Bao'shen recipe to investigate the influence of the drug on expressions of c-Jun N-terminal kinase 1/2(JNK1/2)and Jun-D in the kidney of diabetic mice.Methods: 50 mice were randomly divided into model group and control group(Group C),we use STZ to give the 40 mice of model group an intraperitoneal injection and let them have diabetic nephropathy.Then we divide them into Baoshen' recipe of low dose group(Group D),medium dose group(Group Z),high dose group(Group G),and negative control group(Group Y).After the treatment of 8 weeks,we observe the blood renal fuction,urine renal fuction,relative kidney weight,and renal pathological changes.JNK1/2 and Jun-D mRNA and protein expression of every group by real-time fluorescent quantitative PCR and immunohistochemical analysis.Results:Weight: the negative control group's weight obviously less than the normal control group(P<0.01);the drug intervention groups' weight obviously less than the negative control group(P<0.05);Baoshen' recipe of high dose group's weight was higher than the medium and low-dose group,but there was no obviously significant difference.Relative kidney weight: the negative control group's relative kidney weight obviously more than the normal control group(P<0.01);the drug interventiongroups' relative kidney weight obviously more than the negative control group(P<0.05);Baoshen' recipe of high dose group's weight was lower than the medium and low-dose group,but there was no obviously significant difference.Blood glucose: the model group mice's fasting blood-glucose and postprandial blood-glucose obviously more than the normal group;but there was no obviously significant difference between the model groups.24-hour urine protein quantity:the negative control group's urine protein quantity obviously more than the normal control group(P < 0.01);the drug intervention groups' urine protein quantity obviously less than the negative control group(P<0.01);Baoshen' recipe of high dose group was lower than the medium and low-dose group,but there was no obviously significant difference.Blood renal fuction: the negative control group's BUN and Scr obviously more than the normal control group(P<0.01);the drug intervention groups' BUN and Scr obviously less than the negative control group(P <0.01,P<0.05);Baoshen'recipe of high dose group was lower than the medium and low-dose group,but there was no obviously significant difference.Renal pathological changes: the normal control group's glomerular structure is normal,and has no mesangial proliferation;the negative control group's glomerular is hypertrophic and has been a marked fibrosis;Baoshen'recipe of high dose group's glomerular and tubular structure is basic normal,and there has mild glomerular balloon expansion;the medium and low-dose group's glomerular is hypertrophic,mesangial matrix accumulated and glomerular balloon expanded significantly.JNK1/2 and Jun-D: the JNK1 and Jun-D mRNA and protein expression of the negative control group obviously more than the normal control group(P<0.01);the drug intervention groups' expression obviously less than the negative control group(P<0.01);compared with the medium and low-dose group,Baoshen' recipe of high dose group expression level decreased in the JNK1 and Jun-D mRNA and protein,but there was no obviously significant difference.Conclusion:Baoshen' recipe for diabetic mice kidney plays a protective role,and it can improve diabetic mice kidney pathological changes.The mechanism is probably by impacting JNK-MAPK signal pathway's transduction and protein expression and inhibiting renal fibrosis to improve the effect of diabetic nephropathy in micekidney damage.