Changes of LncRNAs During the Process of Antioxidants Antagonize Cadmium-Induced Oxidative Damage in Islet β Cells

Overview

Journal Cell Biochem Biophys

Specialties Biochemistry
Biophysics
Cell Biology

Date 2024 Feb 24

PMID 38400990

Authors

Rongxian Li

Jiao Dai

Zuoshun He

Shiyan Gu

Affiliations

Soon will be listed here.

Abstract

Long non-coding RNAs (LncRNAs) play important regulatory roles in oxidative damage. Resveratrol, curcumin, and cyanidin are phytogenic antioxidants widely existing in nature and they have been proved to antagonize certain heavy metal-induced oxidative damage in cells. However, can they antagonize oxidative damage induced by cadmium in islet β cells? Are their mechanisms of antagonizing oxidative damage related to LncRNAs? In this study, we first detected the cell viability of each group by CCK8 assay. Next, reactive oxygen species (ROS) were detected by the fluorescent probe. The contents of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD) were detected according to the instructions of corresponding kits. At last, the levels of LncRNAs were detected by fluorescence quantitative real-time polymerase chain reaction (qPCR). The results showed that resveratrol, curcumin and cyanidin were able to reverse the reduction of cell viability induced by cadmium (CdSO). Further determination revealed that SOD activities of the resveratrol+CdSO, curcumin+CdSO, and cyanidin+CdSO treatment groups increased significantly, and ROS levels and MDA contents dramatically decreased when compared with single CdSO-treated group. More importantly, the levels of three CdSO-elevated LncRNAs (NONMMUT029382, ENSMUST00000162103, ENSMUST00000117235) were all decreased and levels of three CdSO-inhibited LncRNAs (NONMMUT036805, NONMMUT014565, NONMMUT065427) were increased after the pretreatment of resveratrol, curcumin and cyanidin. In summary, resveratrol, curcumin and cyanidin may effectly reverse the cadmium-induced oxidative damage and suggest that phytogenic antioxidants may prevent cells from cadmium-induced oxidative damage through changing the levels of LncRNAs.

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