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Published:
Feb 18, 2023DOI:
10.4314/tjpr.v22i1.4Keywords:
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Main Article Content
TRIM8 regulates contrast induced renal cell injury via the TLR4/MyD88/ NF kB pathway
Abstract
Purpose: To investigate the effect of tripartite motif-containing protein 8 (TRIM8) on contrast media-induced injury on kidneys in mice and on human renal tubular epithelial cells.
Methods: Contrast media-induced nephropathy (CIN) model was constructed by injecting meglumine diatrizoate in mice. Small interference technology was used to knock down the expression of TRIM8 in HK-2 cells, while quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) were used to determine the expression levels of the inflammatory factors: TNF-α, TGF-β1, IL-1β, and IL-4. Cell counting kit-8 (CCK-8) assay was employed to determine the cell viability of each group, and TUNEL staining applied to detect apoptosis morphology using a fluorescence microscope. Flow-type Annexin V-FITC/PI double staining and Caspase-3 activity colorimetry were used to observe the changes in apoptosis. Expression of apoptosis factors, including Bax, Caspase3, Caspase9, and anti-apoptotic factor Bcl-2, was determined by qRT-PCR, while expressions of the TLR4/MyD88/NF-kB pathway were determined using Western blot and qRT-PCR.
Results: In CIN group, the kidney tissues significantly expressed IL-1β and Caspase3, while the contents of BUN, SCr, and UP all increased (p < 0.05). At the same time, expression of TRIM8 in the kidney tissues was up-regulated. After knocking down TRIM8, HK-2 cells inhibited the contrast agent-induced apoptosis and inflammation and as well as TLR4/MyD88/NF-kB pathway (p < 0.05).
Conclusion: TRIM8 regulates contrast-induced renal cell damage via TLR4/MyD88/NF-KB pathway. The results of the current study may provide new insights for the development of new treatment strategies for CIN.
