School of Preclinical Medicine, Beijing University of Chinese Medicine, 11 Bei San Huan Dong Road, Chaoyang District, Beijing 100029, China.
BMC Complement Altern Med. 2013 Jul 1;13:152. doi: 10.1186/1472-6882-13-152.
Formaldehyde can induce misfolding and aggregation of Tau protein and β amyloid protein, which are characteristic pathological features of Alzheimer's disease (AD). An increase in endogenous formaldehyde concentration in the brain is closely related to dementia in aging people. Therefore, the discovery of effective drugs to counteract the adverse impact of formaldehyde on neuronal cells is beneficial for the development of appropriate treatments for age-associated cognitive decline.
In this study, we assessed the neuroprotective properties of TongLuoJiuNao (TLJN), a traditional Chinese medicine preparation, against formaldehyde stress in human neuroblastoma cells (SH-SY5Y cell line). The effect of TLJN and its main ingredients (geniposide and ginsenoside Rg1) on cell viability, apoptosis, intracellular antioxidant activity and the expression of apoptotic-related genes in the presence of formaldehyde were monitored.
Cell counting studies showed that in the presence of TLJN, the viability of formaldehyde-treated SH-SY5Y cells significantly recovered. Laser scanning confocal microscopy revealed that the morphology of formaldehyde-injured cells was rescued by TLJN and geniposide, an effective ingredient of TLJN. Moreover, the inhibitory effect of geniposide on formaldehyde-induced apoptosis was dose-dependent. The activity of intracellular antioxidants (superoxide dismutase and glutathione peroxidase) increased, as did mRNA and protein levels of the antiapoptotic gene Bcl-2 after the addition of geniposide. In contrast, the expression of the apoptotic-related gene - P53, apoptotic executer - caspase 3 and apoptotic initiator - caspase 9 were downregulated after geniposide treatment.
Our results indicate that geniposide can protect SH-SY5Y cells against formaldehyde stress through modulating the expression of Bcl-2, P53, caspase 3 and caspase 9, and by increasing the activity of intracellular superoxide dismutase and glutathione peroxidase.
甲醛可诱导 Tau 蛋白和 β 淀粉样蛋白错误折叠和聚集，这是阿尔茨海默病（AD）的特征性病理特征。大脑中内源性甲醛浓度的增加与老年人痴呆密切相关。因此，发现有效药物来抵消甲醛对神经元细胞的不利影响，有利于开发适当的治疗与年龄相关的认知能力下降的方法。
在这项研究中，我们评估了通络救脑（TLJN），一种中药制剂，对人神经母细胞瘤细胞（SH-SY5Y 细胞系）中甲醛应激的神经保护特性。监测 TLJN 及其主要成分（栀子苷和人参皂苷 Rg1）对甲醛存在时细胞活力、细胞凋亡、细胞内抗氧化活性和凋亡相关基因表达的影响。
细胞计数研究表明，在 TLJN 的存在下，甲醛处理的 SH-SY5Y 细胞的活力显著恢复。激光扫描共聚焦显微镜显示，TLJN 和栀子苷（TLJN 的有效成分）可挽救甲醛损伤细胞的形态。此外，栀子苷对甲醛诱导的细胞凋亡的抑制作用呈剂量依赖性。加入栀子苷后，细胞内抗氧化剂（超氧化物歧化酶和谷胱甘肽过氧化物酶）的活性增加，抗凋亡基因 Bcl-2 的 mRNA 和蛋白水平也增加。相比之下，栀子苷处理后凋亡相关基因 - P53、凋亡执行者 - caspase 3 和凋亡起始子 - caspase 9 的表达下调。
我们的结果表明，栀子苷通过调节 Bcl-2、P53、caspase 3 和 caspase 9 的表达以及增加细胞内超氧化物歧化酶和谷胱甘肽过氧化物酶的活性，可保护 SH-SY5Y 细胞免受甲醛应激。
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