目的 探討枸杞多糖（LBP）對小鼠海馬神經(jīng)元細(xì)胞系HT22細(xì)胞缺糖缺氧損傷保護(hù)作用的機(jī)制。方法 采用含1 mmol/L連二亞硫酸鈉的無糖DMEM培養(yǎng)基建立HT22細(xì)胞缺糖缺氧損傷模型，設(shè)對照組、模型組和LBP高、中、低劑量（100、50、25 mg/L）組，以CCK8法檢測細(xì)胞活性，流式細(xì)胞術(shù)檢測檢測細(xì)胞凋亡情況；Western blotting檢測Bcl-2、Bax蛋白表達(dá)情況；利用實時熒光定量PCR（RT-qPCR）檢測TNF-α、NF-κB、I-κBα、Caspase-9基因轉(zhuǎn)錄活性。結(jié)果 與對照組比較，模型組HT22細(xì)胞存活率顯著降低、凋亡率顯著增加（P<0.05）；TNF-α、NF-κB、Caspase-9基因轉(zhuǎn)錄活性顯著上調(diào)，I-κBα基因轉(zhuǎn)錄活性顯著下調(diào)（P<0.05）；Bax蛋白表達(dá)水平顯著升高，Bcl-2的蛋白表達(dá)水平顯著降低（P<0.05）。與模型組比較，LBP各劑量組細(xì)胞存活率顯著上升、凋亡率顯著下降（P<0.05）；TNF-α、NF-κB、Caspase-9基因轉(zhuǎn)錄活性顯著下調(diào)，I-κBα基因轉(zhuǎn)錄活性顯著上調(diào)（P<0.05）；Bax蛋白表達(dá)水平顯著降低，Bcl-2的蛋白表達(dá)水平顯著增高（P<0.05）。結(jié)論 LBP可能是通過下調(diào)TNF-α、NF-κB、Caspase-9基因轉(zhuǎn)錄活性以及Bax蛋白表達(dá)，增強I-κBα基因轉(zhuǎn)錄活性及Bcl-2的蛋白表達(dá)，抑制缺糖缺氧損傷誘導(dǎo)神經(jīng)細(xì)胞凋亡的發(fā)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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寧夏自治區(qū)"十三五"重大科技項目（2016BZ07）；寧夏自然科學(xué)基金項目（NZ13073）；寧夏高等學(xué)?？茖W(xué)項目（NGY2015083）；寧夏醫(yī)科大學(xué)校級項目（XY201713）