摘要
目的以H_2O_2损伤的HT22细胞为体外氧化损伤模型,探讨红景天苷对HT22细胞氧化损伤的作用和机制。方法以0、250、500、1 000μmol/L H_2O_2损伤HT22细胞24 h后,用0、100、400μmol/L红景天苷干预24 h,在倒置显微镜下观察HT22细胞形态学变化。CCK-8比色法检测HT22细胞存活率。免疫荧光组织染色检测超氧化物歧化酶-2(SOD2)的表达。结果加入不同浓度H_2O_2诱导损伤后,HT22细胞生长被抑制,受抑制程度随H_2O_2浓度变化而渐变。H_2O_2损伤后,HT22细胞存活率呈浓度依赖性下降;红景天苷可以逆转HT22细胞存活率的下降,且使细胞形态变化得到改善。染色显示H_2O_2损伤后HT22细胞的SOD2表达增加,但红景天苷干预后SOD2的表达显著降低(P<0.05)。结论红景天苷可以拮抗H_2O_2氧化损伤发挥神经保护作用。
Objective To investigate the effect and mechanism of salidroside on oxidative injury of HT22 cells, and HT22 cells injured by H_2O_2 were used as oxidative injury model in vitro. Methods HT22 cells were injured by 0, 250, 500 and 1 000 μmol/L H_2O_2 for 24 hours, and then given 0, 100 and 400 μmol/L salidroside for 24 hours. The morphological changes of HT22 cells were observed under inverted microscope. CCK-8 colorimetric assay was used to detect the viability of HT22 cell. The expression of superoxide dismutase-2(SOD2) was detected by immunofluorescence staining. Results The growth of HT22 cells were inhibited by adding different concentration of H_2O_2, and the degree of inhibition changed gradually with the concentration of H_2O_2. After H_2O_2 injuryed, the survival rate of HT22 cells decreased in a concentrationdependent manner; salidroside could reverse the decline of HT22 cell survival rate and improve the morphological changes of HT22 cells. The staining showed that SOD2 expression in HT22 cells increased after H_2O_2 injuryed, but decreased significantly after salidroside intervention(P <0.05). Conclusion Salidroside can antagonize oxidative injury induced by H_2O_2 and exert neuroprotective effect.
引文
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