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目的研究芦荟大黄素(AE)对H2O2及甲醛引起的PC12细胞损伤的保护作用。方法将PC12细胞分成AE+H2O2干预组、H2O2损伤组、AE+甲醛干预组、甲醛损伤组、AE对照组和正常对照组6组。各组加入相应药物干预2 h后用不同浓度H2O2或甲醛损伤后进行细胞骨架及凋亡染色、LDH检测。结果 AE+H2O2干预组LDH(67.7±5.5)U/L显著低于H2O2损伤组的(92.0±9.9)U/L(P<0.01);AE+甲醛干预组LDH与甲醛损伤组比较差异无统计学意义(P>0.05);AE+H2O2干预组细胞骨架损伤、凋亡较H2O2损伤组少。结论 AE可通过纠正H2O2诱导的细胞骨架的异常改变,阻滞或延缓PC12细胞的过度凋亡但对甲醛诱导的细胞骨架重排无明显保护作用。
Objective To study the protective effect of aloe-emodin (AE) on H2O2 and formaldehyde-induced PC12 cell injury. Methods PC12 cells were divided into 6 groups: AE + H2O2 intervention group, H2O2 injury group, AE + formaldehyde intervention group, formaldehyde injury group, AE control group and normal control group. Each group was treated with corresponding drugs for 2 h, and then cytoskeleton and apoptosis staining and LDH detection were performed after the cells were injured with different concentrations of H2O2 or formaldehyde. Results The LDH (67.7 ± 5.5) U / L in AE + H2O2 intervention group was significantly lower than that in H2O2 injury group (92.0 ± 9.9 U / L) (P <0.01). There was no significant difference between AE + (P> 0.05). The cytoskeleton injury and apoptosis in AE + H2O2 intervention group were less than those in H2O2 injury group. Conclusion AE can prevent or degrade excessive apoptosis of PC12 cells by H2O2-induced cytoskeletal abnormalities, but have no protective effect on formaldehyde-induced cytoskeletal rearrangements.