论文部分内容阅读
目的研究黄芩苷(BCL)对β-淀粉样蛋白_(25-35)(Aβ_(25-35))引起新生大鼠原代海马神经细胞损伤的保护作用。方法分离新生大鼠海马神经细胞并进行原代培养后,将25μmol·L~(-1)Aβ_(25-35)加入到低、中、高3个质量浓度BCL(25,50,100 mg·m L~(-1))预处理2 h的细胞培养液中,培养24 h后,以四甲基偶氮唑盐(MTT)法检测细胞存活率;用试剂盒测定培养液中丙二醛(MDA)的含量和乳酸脱氢酶(LDH)的释放量及细胞内β-分泌酶的活性。结果模型组的细胞存活率(73.51%)与空白组细胞存活率(100%)比较显著降低,差异有统计学意义(P<0.05);低、中、高3个质量浓度实验组的细胞存活率分别为97.88%,96.94%,94.04%,与模型组比较差异有统计学意义(P<0.05)。与模型组的MDA含量(3.94±0.63)μmol·L~(-1),高质量浓度实验组MDA含量显著降低为(3.02±0.57)μmol·L~(-1),差异有统计学意义(P<0.05);与模型组的LDH的释放量(409.67±93.78)U·L~(-1)比较,中、高2个质量浓度实验组的LDH的释放量分别为(334.41±91.43),(307.65±82.67)U·L~(-1),差异有统计学意义(P<0.05);与模型组的β-分泌酶活性(2.32×104±119.47)u比较,中、高2个质量浓度实验组的β-分泌酶活性分别为(2.31×104±114.78),(2.29×104±99.62)u,差异有统计学意义(P<0.05)。结论 BCL对Aβ_(25-35)引起的新生大鼠原代海马神经细胞的损伤具有一定的保护作用。
Objective To study the protective effect of baicalin (BCL) on primary cultured hippocampal neuronal injury induced by β-amyloid protein (25-35) (Aβ 25-35). Methods After the hippocampal neurons of neonatal rats were isolated and cultured, 25 μmol·L -1 Aβ 25-35 was added to BCL (25, 50, 100 mg · m L) ~ (-1)) for 2 h, the cell viability was detected by MTT assay after 24 h of incubation, and the MDA ) Content and lactate dehydrogenase (LDH) release and intracellular β-secretase activity. Results The cell viability (73.51%) in model group was significantly lower than that in blank group (100%), the difference was statistically significant (P <0.05). The cell survival rates in low, middle and high concentration groups The rates were 97.88%, 96.94% and 94.04%, respectively, which were significantly different from the model group (P <0.05). Compared with the model group, the content of MDA in the experimental group (3.94 ± 0.63) μmol·L -1 was significantly lower than that in the model group (3.02 ± 0.57) μmol·L -1, the difference was statistically significant ( P <0.05). Compared with the release of LDH in the model group (409.67 ± 93.78) U · L -1, the release of LDH in the middle and high concentration groups were (334.41 ± 91.43), (307.65 ± 82.67) U · L -1, the difference was statistically significant (P <0.05). Compared with the model group, the β-secretase activity (2.32 × 104 ± 119.47) u in the middle and high quality The concentrations of β-secretase in experimental group were (2.31 × 104 ± 114.78) and (2.29 × 104 ± 99.62) u, respectively, with statistical significance (P <0.05). Conclusion BCL can protect the primary hippocampal neurons injured by Aβ_ (25-35).