Abstract: Objective To investigate the expression of C-C motif chemokine receptor 2(CCR2) and the numbers of helper T cell 1 / 2 (Th1 / Th2) in renal interstitial fibrosis of rats withIgA nephropathy and their significance. Methods A total of 40 male SD rats were randomly dividedinto 2 groups, each group included 20 rats. Immunoglobulin A (IgA) nephropathy in rats was induced by using a combined treatment of lipopolysaccharide (LPS), modified bovine serum albumin (BSA), and carbon tetrachloride ( CCl4 ). The pathological changes and IgA deposition were observed, the percentage of collagen fibers in renal tissues was calculated, and the Katafuchi score was used to evaluate the degree of tubulointerstitial injury. Western blotting was used to detect the expression level of CCR2 in renal tissues. Serum levels of interleukin-4 ( IL-4) and interferon-γ (IFN-γ) were measured by double-antibody sandwich enzyme-linked immunosorbent assay. Flowcytometry was used to measure the proportion of Th1 / Th2 cells. Results The percentage of collagenfiber area and the Katafuchi score in the model group were significantly higher than those in the control group (P < 0. 05). The expression level of CCR2 in renal tissues, the serum level of IL-4, thenumber of Th2 cells and the ratio of IL-4 / IFN-γ in the model group were significantly higher than those in the control group, while the serum level of IFN-γ and the number of Th1 cells were significantly lower than those in the control group (P< 0. 05). The levels of CCR2 and IL-4 and the ratioof IL-4 / IFN-γ were positively correlated with the collagen fiber area percentage and the Katafuchiscore (P< 0. 05), while the level of IFN-γ was negatively correlated with collagen fiber area percentage and the Katafuchi score ( P < 0. 05). Conclusion The abnormal expression of CCR2 andthe Th1 / Th2 Imbalance are involved in the occurrence and development of renal interstitial fibrosis in IgA nephropathy rats, meanwhile, antagonizing CCR2 and regulating Th1 / Th2 balance may reduce the changes of renal fibrosis in IgA nephropathy rats.

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