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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Ginsenoside Rg1 protects against hydrogen peroxide-induced cell death in PC12 cells via inhibiting NF-kappaB activation.
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Ginsenoside Rg1 protects against hydrogen peroxide-induced cell death in PC12 cells via inhibiting NF-kappaB activation.

机译：人参皂苷Rg1通过抑制NF-κB活化来防止PC12细胞中过氧化氢诱导的细胞死亡。

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摘要

Oxidative stress is a major cause in neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's disease (PD), and cerebral ischemia. Ginsenoside Rg1, a natural product extracted from Panax ginseng C.A. Meyer, has been reported to exert notable neuroprotective activities, which partly ascribed to its antioxidative activity. However, its molecular mechanism against oxidative stress induced by exogenous hydrogen peroxide (H(2)O(2)) remained unclear. In this study, we investigated its effect on H(2)O(2)-induced cell death and explored possible signaling pathway in PC12 cells. We proved that pretreatment with Rg1 at concentrations of 0.1-10 muM remarkably reduced the cytotoxicity induced by 400 muM of H(2)O(2) in PC12 cells by MTT and Hoechst and PI double staining assay. Of note, we demonstrated the activation of NF-kappaB signaling pathway induced by H(2)O(2) thoroughly in PC12 cells, and Rg1 suppressed phosphorylation and nuclear translocation of NF-kappaB/p65, phosphorylation and degradation of inhibitor protein of kappaB (IkappaB) as well as the phosphorylation of IkappaB-kinase complex (IKK) by western blotting or indirect immunofluorescence assay. Besides, Rg1 also inhibited the activation of Akt and the extracellular signal-regulated kinase 1/2 (ERK1/2). Furthermore, the protection of Rg1 on H(2)O(2)-injured PC12 cells was attenuated by pretreatment with two NF-kappaB pathway inhibitors (JSH-23 or BOT-64). In conclusion, our results suggest that Rg1 could rescue the cell injury by H(2)O(2) via down-regulation NF-kappaB signaling pathway as well as Akt and ERK1/2 activation, which put new evidence on the neuroprotective mechanism of Rg1 against the oxidative stress and the regulatory role of H(2)O(2) in NF-kappaB pathway in PC12 cells.
机译：氧化应激是包括阿尔茨海默氏病（AD），帕金森氏病（PD）和脑缺血在内的神经退行性疾病的主要原因。人参皂甙Rg1，是从人参C.A.中提取的天然产物。据报道，迈耶具有显着的神经保护活性，这部分归因于其抗氧化活性。但是，其抗外源性过氧化氢（H（2）O（2））引起的氧化应激的分子机制仍不清楚。在这项研究中，我们调查了其对H（2）O（2）诱导的细胞死亡的影响，并探讨了PC12细胞中可能的信号传导途径。我们证明了用Mg，TT和Hoechst以及PI双重染色法以0.1-10μM的浓度对Rg1进行预处理可显着降低PC12细胞中400μMH（2）O（2）诱导的细胞毒性。值得注意的是，我们证明了由H（2）O（2）在PC12细胞中完全诱导H（2）O（2）诱导的NF-kappaB信号通路的激活，Rg1抑制了NF-kappaB / p65的磷酸化和核易位，磷酸化和kappaB抑制剂蛋白的降解。 （IkappaB）以及IkappaB激酶复合物（IKK）的磷酸化，通过蛋白质印迹或间接免疫荧光测定。此外，Rg1还抑制Akt和细胞外信号调节激酶1/2（ERK1 / 2）的激活。此外，Rg1对H（2）O（2）损伤的PC12细胞的保护通过用两种NF-κB通路抑制剂（JSH-23或BOT-64）进行预处理而减弱。总之，我们的结果表明，Rg1可以通过下调NF-kappaB信号通路以及Akt和ERK1 / 2激活来拯救H（2）O（2）对细胞的损伤，这为Rg1的神经保护机制提供了新的证据。 Rg1的抗氧化应激和H（2）O（2）PC12细胞中的NF-κB通路的调节作用。

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