Effects of IL-33 on renal tubular injury in lupus nephritis through the JAK/STAT signaling pathway

Abstract

Objective To investigate the effects and mechanism of interleukin 33 (IL-33) on renal tubular injury in mice with lupus nephritis. Methods Twelve-week-old female MRL/lpr mice were randomly divided into model group, IL-33 group and solvent control group with 10 rats in each group. Ten female MRL/MP mice of the same age were used as normal control group. The mice in IL-33 group were intraperitoneally injected with 100 μL of phosphate buffer saline (PBS), containing 2 μg of recombinant mouse IL-33, once a day for 14 days. The mice in control group and the model group were intraperitoneally injected with the same dose of PBS. All the mice were sacrificed at 14 weeks of age. Serum creatinine (Cr) and urea nitrogen (BUN) concentrations were determined by serum separation. The urine in 24 hours was collected testing urinary protein creatinine ratio and urinary protein quantification. The contents of E-cadherin, α-SMA, and JAK/STAT pathway signaling proteins, including JAK2, p-JAK2, STAT1, and p-STAT1, were detected by Western blot. Results The BUN, urinary protein creatinine ratio and urine protein level of the IL-33 group were significantly higher than those of the model group (all P 0.05). Conclusions IL-33 can cause tubulointerstitial lesions in lupus mice, and its mechanism may be related to the activation of JAK/STAT pathway. Key words: Lupus nephritis; Tubular interstitial leison; JAK2; Signal transducer and activator of transcription 1