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利用皮质酮诱导PC12细胞损伤模型,研究木豆素A对皮质酮诱导的PC12细胞的保护作用并探讨相应的保护途径。采用100μmol.L1皮质酮与PC12细胞作用48 h,诱导PC12细胞损伤,然后与不同浓度的木豆素A孵育24 h。检测细胞存活率、LDH渗漏量、细胞内Ca2+浓度及caspase-3活性。结果显示,PC12细胞与皮质酮孵育48 h后细胞存活率明显降低,而LDH漏出量、细胞内Ca2+浓度及caspase-3活性均显著升高;木豆素A(4.0、8.0及16.0μmol.L1)具有改善作用,但量效关系不明显。研究表明,木豆素A对皮质酮诱导的PC12细胞损伤具有明显的保护作用,其保护作用可能是通过降低Ca2+浓度及caspase-3活性来实现的。
The injury model of PC12 cells induced by corticosterone was used to study the protective effect of Mucin A on corticosterone-induced PC12 cells and to explore the corresponding protective pathway. PC12 cells were treated with 100μmol.L1 corticosterone for 48 hours to induce PC12 cell injury, and then incubated with different concentrations of mucins A for 24 hours. Cell viability, LDH leakage, intracellular Ca2 + concentration and caspase-3 activity were measured. The results showed that after 48 h of incubation with corticosterone, the viability of PC12 cells was significantly decreased, while the leakage of LDH, the intracellular Ca2 + concentration and the activity of caspase-3 were significantly increased. The inhibitory effects of tachykinin A (4.0, 8.0 and 16.0 μmol.L1 ) Has an improvement effect, but the relationship between the dose-effect is not obvious. Studies have shown that, Mucin A has a significant protective effect on corticosterone-induced injury of PC12 cells, and its protective effect may be achieved by reducing the concentration of Ca2 + and caspase-3 activity.