Effect of circMAT2B on renal tubular epithelial cell damage induced by high glucose through targeting miR-103a-3p
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Abstract
Objective To explore the effect of circMAT2B targeting miR-103a-3p on renal tubular epithelial cell damage induced by high glucose and elucidate its mechanism.Methods Human renal tubular epithelial cells HK-2 were cultured in vitro and HK-2 cells induced by high glucose for modeling cell injury (HG group).Normally cultured HK-2 cells were recorded as Con group.And si-NC,si-circMAT2B,miR-NC,miR-103a-3p mimics,si-circMAT2B,anti-miR-NC,si-circMAT2B and anti-miR-103a-3p were transfected into HK-2 cells and then added 25 mmol/L glucose-treated cells (HG+si-NC group,HG+si-circMAT2B group,HG+miR-NC group,HG+miR-103a-3p group,HG+si-circMAT2B+anti-miR-NC group,HG+si-circMAT2B+anti-miR-103a-3p group).Quantitative real-time polymerase chain reaction (qRT-PCR)was utilized for detecting the expression of circMAT2B and miR-103a-3p;Enzyme-linked immunosorbent assay (ELISA0 for detecting the levels of IL-6 and TNF-α;Flow cytometry for detecting apoptotic rate;Dual luciferase reporter gene experiment for examining the targeting relationship between circMAT2B and miR-103a-3p.Results As compared with Con group,the expression level of circMAT2B and apoptotic rate rose in HG group (P<0.05),the levels of IL-6 and TNF-α spiked (P<0.05)while the expression level of miR-103a-3p dropped (P<0.05).As compared with HG+si-NC group,the levels of IL-6 and TNF-α declined in HG+si-circMAT2B group (P<0.05) and apoptotic rate dropped (P<0.05).circMAT2B could adsorb miR-103a-3p and target its expression.Compared with HG+miR-NC group,the levels of IL-6 and TNF-α declined in HG+miR-103a-3p group (P<0.05)while apoptotic rate dipped (P<0.05).As compared with HG+si-circMAT2B+anti-miR-NC group,the levels of IL-6,TNF-α rose in HG+si-circMAT2B+anti-miR-103a-3p group (P<0.05) and apoptotic rate rose (P<0.05).Conclusions An inhibition of circMAT2B expression may inhibit the secretion and apoptosis of cytoinflammatory factors by negatively regulating the expression of miR-103a-3p,thereby reducing the damage of renal tubular epithelial cells induced by high glucose.
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