Wnt Pathway-based Mechanisms In Rat Renal Tubular Epithelial Cells In Chronic Renal Failure And Kidney Yang Imbalance Steady

Objective To investigate the biological mechanisms of chronic renal failuredeficiency rat renal tubular epithelial homeostasis based Wnt pathway.Method Experimentalanimals were divided into four groups: normal group, adeninegroup, hydrocortisone group and unilateral ureteral ligation (UUO) group, the rats withthe corresponding method of manufacturing models.1) each group of rats was observedafter modeling generally;2) automatic biochemical analyzer to detect the24-hour urineprotein in rat serum creatinine and blood urea nitrogen;3) radioimmunoassay blood ofrats adrenocorticotropic hormone (ACTH), thyroid stimulating hormone (TSH) value;4)immunohistochemistry was used to detect kidney tissue of rats in each group Wnt2b,β-catenin, E-cadherin and expression of α-SMA;5) renal tissue biopsy performed HE,Masson staining pathological changes.Result1)adeninegroup, hydrocortisoneratsappeartodrink more, eat less, polyuria,the gradual emergence of listlessness, weight loss, etc. yang performance.2) comparedwith the normal group, adenine group24h urine protein, serum urea nitrogen andserum creatinine were more significantly increased (P<0.01), UUO group weresignificantly increased (P<0.05), serum urea nitrogen and serum elevated creatininewere more significant (P<0.01); adenine group than in the hydrocortisone group24hurine protein increased significantly (P<0.05).3) compared with the normal group,adenine group, hydrocortisone group had serum TSH levels more significantlydecreased (P<0.01), plasma ACTH were significantly lower (P<0.05).4) pathologyShow: adenine group heaviest damage, UUO group less damage, kidney volumeincreased significantly, pale, widened renal interstitial infiltration of inflammatorycells, fibroblasts and collagen fibers increased, tubular atrophy, tubular thin basementmembrane, renal interstitial edema, the proximal part of the small tube cavity can beseen shedding of epithelial cell necrosis, fibrosis area was spotty distribution. Adeninegroup which also occupy most visible crystalline adenine metabolic glomerular and tubular. Masson staining of tubular structures in model group were significantlydamaged collagen increased significantly. UUO group, significant apoptosis of renaltubular epithelial cells and apoptotic bodies, and consistent with the dynamic changesin the number of tubular atrophy of the law. Model2group and the normal grouppathological normal.5) compared with the normal group, adenine group, E-cadherinmean optical density UUO group were significantly lower (P<0.05), adenine group,α-SMA and β-catenin mean optical density values were UUO group there was asignificant increase (P<0.05), Wnt2b UUO group were significantly increased (P<0.05).Conclusion The presence of chronic renal failure in rats accompanied by adeficiency of adenine-induced performance; hydrocortisone deficiency model rats mereperformance without renal impairment; presence of tubular UUO rats interstitial fibrosiswithout deficiency; tubular epithelial transdifferentiation in the process plays animportant role in chronic renal failure; Wnt/β-catenin pathway is an important signalabnormal renal tubular epithelial cell homeostasis imbalance.