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目的:醛酮还原酶家族1成员B10（AKR1B10）与肝癌的发病机制、早期诊断和预后密切相关，故探讨AKR1B10在肝癌细胞中对细胞周期的影响及其作用机制。方法:采用慢病毒LV-AKR1B10-shRNA感染HepG2细胞，或AKR1B10抑制剂依帕司他处理HepG2细胞，蛋白质印迹法（Western blot）及实时荧光定量PCR法（RT-qPCR）检测AKR1B10的表达水平；通过测定还原型烟酰胺腺嘌呤二核苷酸磷酸在340 nm处吸光度值的下降检测AKR1B10的活性；CCK-8法及流式细胞术检测AKR1B10低表达及不同浓度依帕司他处理HepG2细胞后对细胞增殖和细胞周期的影响；Western blot检测HepG2细胞中p-Rb，细胞周期蛋白D1、E1，p27的蛋白表达水平；两样本均数采用独立样本n t检验。n 结果:AKR1B10在肝癌细胞中表达显著升高，与正常肝细胞相比，HepG2细胞中AKR1B10蛋白相对表达水平为6.71±1.11（n P = 0.012）。依帕司他对AKR1B10的酶活性有明显抑制作用，呈剂量依赖性特点。HepG2细胞中AKR1B10基因被有效沉默，不同浓度AKR1B10抑制剂依帕司他处理HepG2细胞24、48、72 h后均可抑制细胞增殖，促进Gn 0/Gn 1细胞周期阻滞，使p-Rb、周期蛋白D1、E1表达降低，周期素依赖性激酶抑制蛋白p27表达升高。n 结论:抑制AKR1B10表达和活性可通过p27/p-Rb通路，促进HepG2细胞Gn 0/Gn 1细胞周期阻滞。n “,”Objective:Aldo-keto reductase family 1 member B10 (AKR1B10) pathogenesis, early diagnosis and prognosis are closely related with hepatoma. Therefore, this study explores the effect and mechanism of AKR1B10 on cell cycle in hepatoma cells.Methods:HepG2 cells were infected with lentivirus LV-AKR1B10-shRNA or treated with epalrestat, an AKR1B10 inhibitor. The expression level of AKR1B10 was detected by Western blot assay and real-time fluorescence quantitative PCR (RT-qPCR). Decreased AKR1B10 activity was detected by reduced coenzyme II (NADPH) absorbance at 340 nm. The low expression of AKR1B10 and the effect of different concentrations of epalrestat on cell proliferation and cell cycle were detected by CCK-8 method and flow cytometry. The protein expression levels of p-rb, cyclin D1, E1, p27 in HepG2 cells were detected by Western blot. The mean of the two samples was tested using independent sample t-test.Results:AKR1B10 expression level in hepatoma cells was significantly increased compared to normal liver cells, and the relative expression level of AKR1B10 protein in HepG2 cells was 6.71 ± 1.11 (n P = 0.012). Epalrestat was significantly inhibited with the enzymatic activity of AKR1B10 in a dose-dependent manner. AKR1B10 gene in HepG2 cells was effectively silenced. HepG2 cells treated with different concentrations of epalrestat (AKR1B10 inhibitor) for 24, 48 and 72 h had inhibited cell proliferation, promoted G0/G1 cell cycle arrest, reduced the expression of p-Rb, cyclin D1, and cyclin E1 and increased the expression of cyclin dependent kinase inhibitor p27 expression.n Conclusion:AKR1B10 inhibitory expression and activity can promote G0/G1 cell cycle arrest in HepG2 cells through the p27 / p-Rb pathway.