摘要 : This study aimed to investigate the effect and underlying mechanism of long non-coding RNA plasmacytoma variant translocation 1 (PVT1) in lipopolysaccharide (LPS)-induced inflammation injury in HK-2 cells. We established LPS-induc... 展开 This study aimed to investigate the effect and underlying mechanism of long non-coding RNA plasmacytoma variant translocation 1 (PVT1) in lipopolysaccharide (LPS)-induced inflammation injury in HK-2 cells. We established LPS-induced septic acute kidney injury (AKI) model in HK-2 cells. LPS-induced HK-2 cells were transfected with pc-PVT1, pc-NC, si-PVT1 or si-NC. Cell viability and apoptosis rate were detected by MTT assay and Annexin V-FITC/PI Apoptosis Detection kit, respectively. The relationships of PVT1 and inflammatory factors were evaluated by RNA Immunoprecipitation (RIP) assay. The levels of inflammatory factors, apoptosis-related proteins and the expressions of proteins related to c-Jun N-terminal kinase (INK) and nuclear factor-kappa B (NF-kappa B) signaling pathway were detected by ELISA or Western blotting. Compared with cells with pc-NC, cell viability was remarkably decreased and cell apoptosis rate was increased in LPS-induced cells with pc-PVT1 (p <0.05). The levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and IL-1 beta were significantly increased in LPS-induced cells with pc-PVT1 compared with cells with pc-NC (p <0.05). All these changes were reversed in LPS-induced cells with and si-NC (p < 0.05). RTP assay revealed that PVT1 could bind to TNF-a. Furthermore, down-regulated PVT1 remarkably reduced the expressions of p-JNK and p-c-Jun, p-I kappa B alpha and p-p65 (p < 0.05); while increased expressions of these proteins and inflammatory factors induced by up-regulated PVT1 were reversed by JNK or NF-kappa B inhibitors. PVT1 may promote inflammatory response by binding to TNF-a and inhibiting JNK/NF-kappa B signaling pathway in LPS-induced septic AKI cells. (C) 2017 Elsevier B.V. All rights reserved. 收起