Abstract
BackgroundThe aim of this study was to investigate the role of long non-coding RNAs (LncRNAs) antisense non-coding RNA in the INK4 locus (ANRIL) in anti-inflammation of rhein in uric acid nephropathy (UAN) rats.MethodsRat models of UAN were induced by adenine and potassium oxonate. Enzyme-linked immunosorbent assay (ELISA) was performed to assess inflammation factor in serum and supernatant. ANRIL mRNA level was detected using real-time reverse transcription PCR (qRT-PCR). Immunostaining was used to observe pathological changes of renal tissues in rats.ResultsANRIL and inflammatory factor levels were highly expressed in patient with UAN. Furthermore, rhein showed an observable effect on anti-inflammatory and renal protection in UAN rats, rhein inhibited expressions of ANRIL in vivo or in vitro. Besides, ANRIL-mediated inflammatory response attenuated protective effect of rhein.ConclusionsANRIL-mediated inflammatory response attenuated the protective effect of rhein in UAN rats. This study showed an understanding of the role and mechanism of ANRIL in UAN, which provides a new target and therapy for the prevention and treatment of UAN.
Highlights
The aim of this study was to investigate the role of long non-coding RNAs (LncRNAs) antisense noncoding RNA in the INK4 locus (ANRIL) in anti-inflammation of rhein in uric acid nephropathy (UAN) rats
ANRIL and inflammatory factors were highly expressed in patient with UAN Serum inflammatory factors in patient with UAN were detected using Enzyme-linked immunosorbent assay (ELISA)
The results showed that TNF-α, IL-1β, IL-6 and IL-8 level was significantly upregulated in patient with UAN compared to that in normal control (P < 0.01, Fig. 1a)
Summary
The aim of this study was to investigate the role of long non-coding RNAs (LncRNAs) antisense noncoding RNA in the INK4 locus (ANRIL) in anti-inflammation of rhein in uric acid nephropathy (UAN) rats. Serum urate levels at a consistently high concentration can cause urate crystal deposition in ducts and/or in the interstitium, and stimulates a series of inflammatory responses to further develop kidney disease [2, 3], named Uric acid nephropathy (UAN). Long non-coding RNA ANRIL (CDKN2B antisense RNA 1) in the INK4 locus is transcribed as a 3.8-kb-long RNA in the opposite direction of the INK4B-ARFINK4A gene cluster [15].
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