ABSTRACT
ObjectiveTo explore the underlying mechanism of Tripterygium wilfordii polyglycoside tablets （TWPT） in the prevention and treatment of kidney injury in diabetic nephropathy （DN） through the nuclear factor of activated T-cells 2（NFAT2）/cyclooxygenase-2（COX-2） pathway. MethodForty-two male SD rats of SPF grade were selected and randomly divided into a normal group （n=8） and an experimental group （n=34） after one week of adaptive feeding. The rats in the normal group were fed conventionally. The DN model was established in rats of the experimental group by intraperitoneal injection of streptozotocin （STZ） following one week of feeding on a high-fat and high-glucose diet. After the death and failure cases during modeling were eliminated， the remaining 24 model rats were randomly divided into model group， valsartan （8.33 mg·kg-1·d-1） group， and TWPT （5 mg·kg-1·d-1） group. Rats in normal group and model group were given equal amounts of normal saline by gavage. After six weeks， body weight was measured and urine samples were collected. Blood samples were collected from the abdominal aorta， and then the rats were sacrificed for sampling. Biochemical indicators， such as serum blood urea nitrogen （BUN）， serum creatinine （SCr）， alanine aminotransferase （ALT）， blood lipid， blood glucose， and 24-hour urine total protein （24 h UTP）， were determined. Hematoxylin-eosin （HE） staining and Masson staining were used to observe the pathology of the kidney. Enzyme-linked immunosorbent assay （ELISA） was used to detect NFAT2 and COX-2 expression levels in the serum. Western blot and Real-time fluorescence quantitative polymerase chain reaction（Real-time PCR）were adopted to detect NFAT2， COX-2 protein and mRNA expression in kidney tissues， respectively. ResultCompared with the normal group， the model group showed elevated 24 h UTP， BUN， SCr， CHO， TG， and FBG， increased serum NFAT2 and COX-2 production and expression （P<0.01）， and elevated protein and mRNA expression of NFAT2 and COX-2 in kidney tissues （P<0.01）. In addition， the pathology of the kidney showed enlarged glomeruli， mild proliferation of mesangial cells， and widened mesangial stroma. Compared with the model group， the TWPT group showed decreased 24 h UTP， BUN， SCr， CHO， TG， and FBG （P<0.05，P<0.01）， basically normal glomerular morphology， decreased expression of serum NFAT2 and COX-2 （P<0.01）， and down-regulated protein and mRNA expression of NFAT2 and COX-2 in kidney tissues （P<0.01）. ConclusionTWPT can alleviate 24 h UTP in DN model rats， protect renal function， and improve renal pathology， and its mechanism of action may be related to the down-regulation of NFAT2/COX-2 expression in the serum and kidney tissues.
ABSTRACT
Objective To explore the clinical and pathological features, treatment, and prognosis of capillary proliferative purpura nephritis (DEP-HSPN) in children.MethodsThe clinical data of 19 children diagnosed with DEP-HSPN were retrospectively analysis. Fifty-five children diagnosed with HSPN by renal biopsy were randomly selected as control group. ResultsThe average age was 10.6±2.6 years old, and the average course of disease were 19.4±7.4 days before renal biopsy in 19 children with DEP-HSPN (14 males and 5 females) who make up 3.92% of anaphylactic purpura nephritis children conifrmed by renal biopsy in the same period. In these 19 children, there were 10 cases having nephrotic syndrome and 9 case having hematuria and proteinuria type, all of whom were received immunosuppressive therapy. Finally, 14 cases achieved completely remission and 5 cases had partly remission. All of their classiifcations of renal pathology wereⅢb levels, accompanied with 6.38% to 36.36% of crescents. Compared with 55 age and sex matched children with renal pathology classiifcation ofⅢb, the DEP-HSPN children had shorter disease course, higher level of proteinuria, and lower pathological score of chronic renal injury (P all?