中文摘要：

目的：探讨二氢杨梅素（Dihydromyricetin，DMY）对硝普钠（SNP）诱导的PCI2细胞氧化损伤的保护作用及机制。方法：建立硝普钠诱导的PCI2细胞氧化损伤模型，采用噻唑蓝（MTT）比色法及Hoeehst染色法考察二氢杨梅素对PCI2细胞活力的影响；DCFH—DA荧光探针检测细胞间活性氧（ROS）的含量；蛋白免疫印迹（Westem blot）法检测Akt和ERK 1／2的磷酸化水平。结果：MTT显示硝普钠剂量依赖性损伤PCI2细胞，而二氢杨梅素可保护硝普钠所致的细胞损伤。ROS结果表明二氢杨梅素能显著降低硝普钠诱导的活性氧增加。丝裂原活化蛋白激酶（MAPK）抑制剂PD98059和磷脂酰肌醇3一激酶（P13K）抑制剂LY294002可抑制二氢杨梅素对硝普钠诱导细胞损伤的保护作用。Western blot结果显示LY294002和PD98059可分别抑制二氢杨梅素对Akt和ERK1／2的磷酸化作用。结论：二氢杨梅素对硝普钠诱导的PCI2细胞损伤具有显著的保护作用，这一作用可能是通过上调Akt和ERK1／2的活性来介导的。

英文摘要：

Objective：To study the protective effect and possible mechanisms of Dihydromyricetin（DMY） on PC12 cells injury in- duced by sodium nitroprusside（SNP）. Methods：SNP toxicity cellular model was established using PC12 cells treated with SNP. Cell via- bility was determined by M3T assay. The apoptosis of treated cells was detected by Hoechst Staining. Effect of DMY on accumulation of ROS in PC12 cells induced by SNP was detected by fiuorometric analysis. The pathways involved were studied by kinase specific inhibi- tors;The level of phosphorylated Akt and ERK1/2 was detected by Western blot with specific phosphor-antibodies. Resuhs：SNP in- duced the apoptosis of PC12 cells in a dose-dependent manner. DMY dose-dependently protected PC12 cells from injury induced by SNP. Hoechst staining indicated that SNP decreased the number of viable cells and induced shrinkage and aggregation of the nucleus, whereas DMY attenuated the toxic effects of SNP. The level of ROS induced by SNP in PC12 cells was decreased gradually by DMY. PI3K specific inhibitor LY294002 and the MAPK pathway specific inhibitor PD98059 attenuated the protective effect of DMY on SNP-induced injury of PC12 cells. However, the effect of DMY could be blocked by LY294002 and PD98059 respectively. Conclusion： DMY possesses protective effect against apootosis induced by SNP in PC12 cells, and its mechanisms may be partially related with Akt and ERKI/2 signaling.