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  • LncRNA NEAT1 regulated inflammation and apoptosis in a rat model of sepsis-induced acute kidney injury via MiR-27a-3p/TAB3 axis.

LncRNA NEAT1 regulated inflammation and apoptosis in a rat model of sepsis-induced acute kidney injury via MiR-27a-3p/TAB3 axis.

Bioscience, biotechnology, and biochemistry (2020-07-24)
Jiasheng Wang, Yong Chen, Ze Tang, Dabi Hu, Caoyuan Yao, Lei Yang
ABSTRACT

This study explored the mechanism of NEAT1 in sepsis-induced AKI rats. Cecal ligation punctures (CLP)-induced AKI rats were injected with siRNA-NEAT1 lentivirus. Kidney histopathology and apoptosis were evaluated via hematoxylin-eosin and TUNEL staining, respectively. ELISA determined the levels of Blood urea nitrogen (BUN), serum creatinine (SCr), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), TNF-α, Interleukin (IL)-1β, and IL-6. Colorimetry measured malondialdehyde (MDA), superoxide dismutase (SOD) activities. qPCR analyzed NEAT1, miR-27a-3p, TAB3, Bcl-2, and Bax expressions. siNEAT1 reversed the promotive effect of CLP on kidney histopathological injury, and BUN, SCr, NGAL, KIM-1, TNF-α, IL-1β, IL-6, MDA, and Bax levels and apoptosis, but raised CLP-downregulated SOD and Bcl-2 levels. NEAT1 sponged miR-27a-3p which targeted TAB3. siNEAT1 upregulated miR-27a-3p and downregulated TAB3 expression. TAB3 overexpression reversed the inhibitory effect of siNEAT1 on the LPS-induced apoptosis of HK-2 cells. siNEAT1 alleviated sepsis-induced AKI in rats and LPS-induced sepsis of cells via miR-27a-3p/TAB3 axis.

MATERIALS
Product Number
Brand
Product Description

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Isopropyl alcohol, ≥99.7%, FCC, FG
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Formalin solution, neutral buffered, 10%, case of 48 × 15 mL, histological tissue fixative
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Eosin Y, Dye content ~99 %
BRAND® slide box, Holds 5 or 10 x slides 76x26 mm
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Ethyl alcohol, Pure, 200 proof, for molecular biology
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Hematoxylin
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DAPI, for nucleic acid staining