Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 85, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2020.106620
Keywords
lincRNA-Cox2; miR-150-5p; STAT1; Rhein; Inflammatory injury; Uric acid nephropathy
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Rhein has protective effect on uric acid nephropathy (UAN). This article aims to demystify the mechanism of function of rhein in UAN. Mouse kidney epithelial cell line (TCMK-1) was incubated with uric acid (UA) to induce inflammatory injury. Then, the TCMK-1 cells were treated with rhein. The relationships among lincRNA-Cox2, miR-150-5p and STAT1 were evaluated by luciferase reporter assay. CCK8 and flow cytometry were performed to detect cell proliferation and apoptosis. The levels of IL-6, IL-1 beta and TNF-alpha were investigated by enzyme linked immunosorbent assay. Western blot and quantitative real-time PCR were performed to examine the expression of genes and proteins. We found that UA suppressed proliferation and enhanced apoptosis and the levels of IL-6, IL-1 beta and TNF-alpha of TCMK-1 cells, which was effectively improved by rhein treatment. Furthermore, lincRNA-Cox2 overexpression caused an increase of apoptosis and inflammatory factors in the rhein-treated TCMK-1 cells. LincRNA-Cox2 regulated STAT1 expression by sponging miR-150-5p. And lincRNA-Cox2 promoted apoptosis and inflammatory injury of TCMK-1 cells by regulating miR-150-5p/STAT1 axis. In summary, our studies demonstrate that rhein has a protective effect against UAN by inhibiting renal inflammatory injury via lincRNA-Cox2/miR-150-5p/STAT1 axis.
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