目的 探讨枸杞多糖（LBP）对小鼠海马神经元细胞系HT22细胞缺糖缺氧损伤保护作用的机制。方法 采用含1 mmol/L连二亚硫酸钠的无糖DMEM培养基建立HT22细胞缺糖缺氧损伤模型，设对照组、模型组和LBP高、中、低剂量（100、50、25 mg/L）组，以CCK8法检测细胞活性，流式细胞术检测检测细胞凋亡情况；Western blotting检测Bcl-2、Bax蛋白表达情况；利用实时荧光定量PCR（RT-qPCR）检测TNF-α、NF-κB、I-κBα、Caspase-9基因转录活性。结果 与对照组比较，模型组HT22细胞存活率显著降低、凋亡率显著增加（P<0.05）；TNF-α、NF-κB、Caspase-9基因转录活性显著上调，I-κBα基因转录活性显著下调（P<0.05）；Bax蛋白表达水平显著升高，Bcl-2的蛋白表达水平显著降低（P<0.05）。与模型组比较，LBP各剂量组细胞存活率显著上升、凋亡率显著下降（P<0.05）；TNF-α、NF-κB、Caspase-9基因转录活性显著下调，I-κBα基因转录活性显著上调（P<0.05）；Bax蛋白表达水平显著降低，Bcl-2的蛋白表达水平显著增高（P<0.05）。结论 LBP可能是通过下调TNF-α、NF-κB、Caspase-9基因转录活性以及Bax蛋白表达，增强I-κBα基因转录活性及Bcl-2的蛋白表达，抑制缺糖缺氧损伤诱导神经细胞凋亡的发生。

Objective s To observe the protective effects of Lycium barbarum polysaccharides (LBP) on oxygen-glucose deprived mouse hippocampal neurons. Methods Cultured mouse hippocampal neurons exposed to 1 mmol/LNa₂S₂O₄ to establish oxygenglucose deprivation model, assigned to control group, model group and LBP group with different doses (100, 50 and 25 mg/L), the cell activity rate was measured by CCK8 assay, and the apoptosis rate was analyzed by Flow Cytometry; the protein expression of Bcl-2 and Bax was measured by Western blotting; RT-qPCR assay was used to evaluate the mRNA expression of TNF-α, NF-κB, I-κBα, Caspase-9. Results Compared with control group, HT22 cell survival rate and apoptosis rate in model group were significantly reduced (P<0.05); TNF-α, NF-κB, caspase-9 gene transcription activity was significantly increased, I-κBα gene transcription activity was significantly decreased (P<0.05); Bax protein expression level was significantly increased, Bcl-2 protein expression level was significantly decreased (P<0.05). Compared with control group, LBP can significantly increase cell viability (P<0.05); reduce the cell apoptosis rate (P<0.05); the expression of TNF-α, NF-κB, Bax and Caspase-9 were effectively down regulated; induce an increase of I-κBα mRNA leve and Bcl-2 protein level (P<0.05). Conclusion LBP have significantly protective effects on oxygen-glucose deprivation, such protective effects may be mediated by its action on the downstream TNF-α, NF-κB, Bax, Caspase-9, and up-regulation of Bcl-2 and I-κBα.

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宁夏自治区"十三五"重大科技项目（2016BZ07）；宁夏自然科学基金项目（NZ13073）；宁夏高等学校科学项目（NGY2015083）；宁夏医科大学校级项目（XY201713）