Changes of aryl hydrocarbon receptor in cardiac hypertrophy induced by high glucose in vitro / 中国病理生理杂志

ABSTRACT

AIM:To investigate the changes of aryl hydrocarbon receptor (AhR) in the process of cardiomyo-cyte hypertrophy induced by high glucose , and to explore its potential mechanisms .METHODS: The rat cardiomyocytes (H9c2 cells) were divided into normal glucose group , high glucose group, DMSO group and resveratrol (an AhR antago-nist) group.The content and distribution of AhR were observed with immunofluorescence staining .The myocardial cells were stained with rhodamine-labeled phalloidin to visualize cytoskeleton , and the cell surface area were determined after im-aging by fluorescence microscopy .The generation of reactive oxygen species ( ROS) in the cardiomyocytes was measured u-sing a fluorescent probe DCFH-DA.The mRNA expression of AhR , CYP1A1, atrial natriuretic peptide ( ANP) and brain natriuretic peptide ( BNP) were evaluated by real-time quantitative PCR ( RT-qPCR).The protein levels of AhR, CYP1A1, ANP and BNP were assessed by Western blot .RESULTS:AhR was constitutively presented in the cytosol un-der normal-glucose condition and was translocated to the nuclei under high-glucose condition .High glucose induced cardiac hypertrophy , and increased ROS generation .Significant reductions in the cell size and ROS generation were observed after treated with resveratrol.The expression of AhR, CYP1A1, ANP and BNP at mRNA and protein levels in high glucose group was increased as compared with normal glucose group and resveratrol group , and the above-mentioned indexes signifi-cantly decreased in resveratrol group as compared with DMSO group .CONCLUSION: High glucose-induced cardiac hy-pertrophy increases AhR expression , which may be involved in the maintenance of glucose homeostasis in the cardiomyo-cytes.AhR translocation to the nucleus induced by high glucose results in the increases in CYP 1A1 expression and ROS generation, which may be an important mechanism of high glucose-induced cardiomyocyte hypertrophy .