为探究枸杞多糖对肝癌模型大鼠癌组织细胞凋亡的干预效果及作用机制。选取45只SD健康雄性大鼠，5只作为正常组，其余40只建立肝癌模型，分为模型组、药物对照组、低、高浓度组，并分别进行干预。观察各组大鼠细胞增殖、凋亡、周期分布情况，检测PTEN、p-Akt、mTOR、Bcl-2、Bax、caspase3表达。研究结果显示，高浓度组G1期细胞比例为57.59%，高于模型组、药物对照组、低浓度组（p<0.05）。高浓度组大鼠增殖率为8.53%，凋亡率为47.68%，均优于模型组、药物对照组和低浓度组。高浓度组大鼠PTEN相对表达量为0.98，p-Akt、mTOR相对表达量分别为1.05、1.11，高浓度组大鼠Bcl-2、caspase3相对表达量分别为1.26、1.19，Bax相对表达量为0.98，干预效果均优于药物对照组和低浓度组（p<0.05）。实验结果表明，在枸杞多糖的干预下，肝癌大鼠癌组织肿瘤细胞增殖、凋亡及周期分布受到明显调控，PTEN、p-Akt、mTOR、Bcl-2、caspase3、Bax表达受到明显的调控，说明枸杞多糖能够阻滞肝癌组织细胞周期分布，抑制肝癌组织细胞增殖，促进细胞凋亡，为肝癌的临床治疗提供一定的理论依据。

To investigate the effect and mechanism of Lycium barbarum polysaccharides on apoptosis of model rats with hepatocarcinoma. Forty-five healthy male SD rats were selected, with 5 as the normal group, and the remaining 40 rats divided into liver cancer model group, drug control group, low- and high-dose intervention groups. The cell proliferation, apoptosis and cycle distribution of the rats in each group were observed, and the expressions of PTEN, p-Akt, mTOR, Bcl-2, Bax and caspase-3 were detected. The results showed that the proportion of cells at the G1 phase in the high-dose intervention rats was 57.59%, which was higher than those of the model group, drug control group and low-dose intervention group (p<0.05). The proliferation rate and apoptotic rate of the rats in high-dose intervention group were 8.53% and 47.68%, respectively, which were better than those of the model group, drug control group and low-dose intervention group. The relative expression of PTEN, p-Akt, mTOR, Bcl-2, Caspase-3 and Bax in the high-dose treated rats was 0.98, 1.05, 1.11, 1.26, 1.19 and 0.98, respectively. The interventional effect was greater than that of the drug control group and low-dose intervention group (p<0.05). The results showed that the Lycium barbarum polysaccharides could significantly regulate the proliferation, apoptosis and cell cycle distribution, as well as the expression of PTEN, p-Akt, mTOR, Bcl-2, caspase 3 and Bax in the rats with hepatocarcinoma. Lycium barbarum polysaccharides could block the cell cycle distribution, inhibit the proliferation and promote cell apoptosis of hepatocarcinoma cells, which provides a theoretical basis for the clinical treatment of hepatocarcinoma.

国家自然科学基金面上项目（81773507）；淮安市自然科学研究计划项目（HAB201717）