| cytokines in renal tissue during renal interstitial fibrosis in rat. Then we can filter out more potential cytokines related with renal interstitial fibrosis. After through further research, we can make in-depth understanding of the role of inflammatory factors. It will help us to clarify the mechanism of renal interstitial fibrosis, and thus provide a new direction for the prevention and treatment of chronic kidney disease. Methods : 60 SD male rats were randomly assigned to sham operation group (SOR) and unilateral ureteral obstruction group (UUO). The 5 rats of each group were randomly selected and killed at 5,7,11,14 and 21 day after operation. We collected 5ml blood to examine the changes of renal function, collected obstructed kidney to observe pathological changes. By using above-mentioned method, the most representative time for the change of kidney in interstitial renal fibrosis has been determined. Then we used the kidney tissue of this time for detection by cytokine antibody microarray, to detect the changes of 19 kinds of cytokines in rats' kidneys during the formation of renal interstitial fibrosis. Base on this, we used simvastatin for drug intervention. The effect of simvastatin on expression of Fractalkine and CX3CR1 receptor has been observed. 15 male rats were randomly assigned to three groups: Sham operation group(SOR),UUO group,Operation plus simvastatin group. The rats in the treatment Abstract: Objective: Antibody microarray technique was been used for detection of obstruction,histological observations of renal tissues revealed that the degree of renal tubulointerstitial fibrosis increased gradually, and the pathological change of obstruction kidney is the most typical at 14th after UUO。By using antibody microarray technique for detection of 19 kinds of inflammatory factors in the renal tissue, there are 17 kinds of inflammatory factors increase or decrease at different levels(P<0.05). We find the expression levels of Fractalkine, GM-CSF, IL-1α, IL-1β, IL-6, IFN-γ, LIX, Leptin, MCP-1, MIP-3α, TIMP-1 and TNF-αwere increased, especial MCP-1,Fractalkine and TIMP-1 (P<0.05); IL-4 and IL-10 were decreased comparing with SOR-operation controls(P<0.05). The expression levels of VEGF, CINC-2 and CINC-3 were increased frist and then decreased.(P<0.05); CNTF andβ-NGF did not change significantly。compared with SOR group, the renal fibrosis of UUO group and operation plus simvastatin group were Obviously at 14th day after simvastatin. The degree of renal fibrosis in the treatment groups was much lower than that in UUO group after surgery. Conclusion:Unilateral ureteral obstruction can rapidly establish the ideal model for kidney cell transdifferentiation and interstitial fibrosis of rat, and the degree of renal interstitial fibrosis will aggravate with the progressive of renal function decline. The results of antibody microarray showed the groups were intragastically given simvastatin (5mg/d) after the operation of left ureter ligature. The rats in each group were killed at 14 days after operation and collected obstructed kidney to observe pathological changes. Results: Compared with those of SOR group, the pathological changes of early fibrosis in Kidney have been observed in UUO group. The renal function was decreased gradually with time of ureteral obvious change for MCP-1, Fractalkine and TIMP-1. This indicated that these three inflammatory factors played the important role for promoting fibrosis in the process of renal interstitial fibrosis. Fractalkine was selected as the important cytokines, but the investigation of mechanism is awaiting further study. The result indicated simvastatin may inhibit the expression of Fractalkine and CX3CR1 receptor, so delay the progress of renal interstitial fibrosis. |
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