Liver fatty acid binding protein protects renal function through down-regulation of oxidative stress in IgA nephropathy

IgA nephropathy (IgAN) is the most common type of primary glomerulonephritis worldwide and there is still no specific treatment for this disease. Increasing evidence has indicated that overload oxidative stress is closely related to IgAN. Liver fatty acid binding protein (L-FABP) has certain anti-oxidant properties. However, its role in IgAN has not been investigated. In this study, we evaluated the protective role of hL-FABP against IgAN on a transgene mouse model. hL-FABP was introduced in wild type (WT) and ddY (IgAN mice) mice and consequently transgene mice (Tg-WT and Tg-ddY) were generated. IgA measurement in kidney showed that Tg-ddY mice could effectively reduce IgA accumulation in the kidney. Blood urea nitrogen and creatinine were also decreased in Tg-ddY mice, indicating that renal function was protected. RT-PCR and western blot analysis of oxidative stress-related gene expression revealed that hL-FABP could decrease the expression of oxidative genes 4-HNE, HO-1, MCP-1, FN, TNF-alpha on both mRNA and protein levels. Taken together, our results here indicate that hL-FABP has a protective role in renal function against IgAN via reduction of oxidative stress by down-regulation of oxidative gene expression. The results herein could provide useful information for the understanding of IgAN pathogenesis as well as the development of IgAN specific treatments.