Aim To investigate whether liver X recep- tors attenuate high glucose-induced apoptosis in H9C2 cells through inhibiting nuclear factor-NF-κB.Methods The lentiviral vector of LXRs was constructed and H9C2 cells cultured in high glucose were infected.The H9C2 cells were divided into 6 groups:control group (5.5 mmol·L -1 glucose),mannitol group(5.5 mmol ·L -1 glucose +27.5 mmol·L -1 mannitol),high glu-cose group(33 mmol·L -1 glucose),green fluorescent protein(GFP)group LXRαgroup,and LXRβgroup. The inhibition rate of H9C2 cells,the mRNA of Bax, Bcl-2,the protein content of NF-κB,Bax,Bcl-2, cleaved caspase-3,and the cell apoptosis were com-pared among these groups.Results LXRs overexpres-sion significantly attenuated high glucose-induced in-crease in Bax NF-κB,cleaved caspase-3 and cell ap-optosis(P <0.05),and increased high glucose-induced decrease in Bcl-2.Conclusion Liver X receptors at-tenuate high glucose-induced apoptosis in H9C2 cells through NF-κB signaling pathway.%目的：探讨肝 X 受体（LXRs）是否通过抑制核转录因子κB（NF-κB）表达减轻高糖诱导的 H9C2细胞凋亡。方法LXRs 过表达慢病毒载体的构建及转染高糖培养的 H9C2细胞；实验分组：对照组（5.5 mmol·L －1葡萄糖）、甘露醇组（5.5 mmol·L －1葡萄糖＋27.5 mmol·L －1甘露醇）、高糖组（33 mmol·L －1葡萄糖）、GFP 组、LXRα组、LXRβ组。检测细胞增殖抑制率，Bax mRNA、Bcl-2 mRNA 表达，NF-κB、Bax、Bcl-2、Cleaved caspase-3蛋白量，细胞凋亡率。结果过表达LXRs 组明显降低高糖诱导的 Bax、NF-κB 及 Cleaved caspase-3蛋白表达及细胞凋亡（P ＜0.05），上调由高糖抑制 Bcl-2的表达（P ＜0.05）。结论LXRs 通过 NF-κB 信号通路减轻高糖诱导的 H9C2细胞凋亡。
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