Epigallocatechin gallate attenuates uric acid-induced injury in rat renal interstitial fibroblasts NRK-49F by up-regulation of miR-9.

Abstract

Hyperuricemia is a common symptom in chronic kidney disease (CKD) and uric acid (UA) was observed to be elevated in CKD. Epigallocatechin gallate (EGCG) was reported to have multiple protective functions in inflammatory process. In this study, we investigated the effects of EGCG in UA-treated NRK-49F cells. NRK-49F cells induced by UA were treated with EGCG and/or transfected with microRNA-9 (miR-9) inhibitor or its negative control (NC). Cell viability and cell apoptosis were detected by Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. In addition, the expression of cell survival- and fibrosis-related factors was measured by qRT-PCR and Western blot, respectively. Concentrations of inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA). Increasing cell viability (p < 0.01) and decreasing cell apoptosis (p < 0.01), cell fibrosis (p < 0.01) and inflammatory cytokines (p < 0.05) were observed by administration of EGCG in UA-treated cells. In addition, miR-9 was significantly up-regulated by EGCG (p < 0.05 or p < 0.001). Furthermore, transfection with miR-9 inhibitor impaired the protective functions of EGCG in UA-treated NRK-49F cells (p < 0.05 or p < 0.01). EGCG significantly down-regulated expression of IκBα, p65, janus kinase (JAK) 2 and signal transducers and activator of transcription (STAT) 3 (all p < 0.05). EGCG attenuates UA-induced injury in NRK-49F cells by up-regulation of miR-9 and might by inactivation of NF-κB and JAK-STAT signal pathways.