ABSTRACT
Objective To investigate the association between stem cell factor (SCF) expression and tubulointerstitial fibrosis in the kidney of rat model with uric acid nephropathy. Methods Thirty-six Wistar rats were randomly divided into model group and control group. The rats in the model group were fed with adenine by lavage at a dose of 150 mg·kg-1·d-1, and the rats in the control group were fed with normal saline by lavage at equal volume. Six rats from each group were sacrificed respectively at week 4, 8 and 12. The mRNA levels of SCF and ColⅠin the kidney were detected by real-time fluorescence quantitative polymerase chain reaction (PCR), and their protein levels and infiltrated Mast cell (MC) were measured by immunohistochemistry. The difference and correlation of each index among different time points and groups were compared. The differences between the two groups were tested by t-test, multiple data were tested by one-way analysis of variance (ANOVA) and the correlation was analyzed by Pearson's correlation. Results ①The serum uric acid (SUA) [week 4, 8, 12: (302 ±41))μmol/L, (424 ±61) μmol/L, (518 ±57) μmol/L], creatinine[week 4, 8, 12:(151±9)μmol/L, (219±15)μmol/L, (299±21)μmol/L], urea nitrogen [week 4, 8, 12:(26.7±3.7) mmol/L, (40.3 ±5.7) mmol/L, (61.9 ±9.4) mmol/L], urine protein/creatinine (Up/Ucr) [week 4, 8, 12: (0.71 ±0.10) mmol/L, (1.18 ±0.11) mmol/L, (1.78 ±0.13) mmol/L] and the expressions of SCF mRNA [week 4, 8, 12: (1.19 ± 0.41), (1.69 ±0.63), (2.21 ±0.97)} and SCF protein [week 4, 8, 12: (1.42 ±0.33), (6.02 ±1.81), (10.03 ±2.69)] in nephridial tissue of model group's rats were significantly higher compared to the control group (all of t value>4.59, P<0.01), and the indexes were increasing gradually as the lavage going on. ②The expression of SCF was correlated with collagenⅠ, degree of renal interstitial injury, urine nitrogen, serum creatinine and UP/Ucr(At week 4, r=0.53, 0.42, 0.40 and 0.51 respectively;at week 8, r=0.60, 0.59, 0.41 and 0.39 respectively;at week 12, r=0.74, 0.61, 0.56 and 0.39 respectively, all of P value<0.05). ③ Compared with control group, the number of infiltrated MC was significantly higher in the model group, and was positively correlated with the expression of SCF (r=0.91, P<0.01). Conclusion Compared with the control group, the expression of SCF and the number of infiltrated MC in the renal interstitium are evidently increased, and are increasing gradually as the lavage going on and the deteriorating of renal interstitial damage. These results suggest that both may play important roles in the occurrence and development of uric acid nephropathy.
ABSTRACT
The relationship between diabetes and osteoporosis has gradually become a new research hotspot , but is still much controversy .High concentration of blood glucose can be bond to varieties of proteins in vivo and form glycosylation end products in col -lagen tissue and reduce bone strength , besides it can inhibit RANKL induced osteoclast formation and bone resorption by repressing redox-sensitive NF-kappa B activity .A series of diabetes mellitus complications can induce less local bone nutrition supply and calcium and phosphorus sorption , reduce muscle tension and bone mineral density , which leads to the increase of fracture risk .Type 2 diabetes patients with overweight or obesity often have increased secretion of inflammation factors , adiponectin and leptin , which promotes the formation of osteoclasts and encourages bone marrow stromal stem cells to differentiate into adipocytes ;On the other hand , adiponectin and leptin can facilitate osteoblasts proliferation , differentiation and activity , and promotes bone formation .This article will discuss how diabetes works on bone metabolism and the underlying pathophysiological and physiological mechanism .