Accumulating evidences demonstrated that Reactive Oxygen Species (ROS) may lead to serious damages to numerous cellular biomolecules, consequently resulting in the development of several neurological diseases. Diclofenac (Dic), the most widely preferred non-steroidal anti-inflammatory drug (NSAID) induces apoptosis by an alteration in function of mitochondria and creation of ROS. Chrysin (Chr) is a naturally active component that is found in numerous plants and bee products and retains strong neuroprotective and antioxidant properties. However its effect of Dic induced injury on SH-SY5Y neuron cells have not been investigated to date. The goal of present research was to study the molecular mechanisms of Chr protection from oxidative injury caused by Dic in SH-SY5Y cells. Dic induced significant toxicity on the cells and this effect was reversed by pre-treatment with Chr. Dic triggered a noteworthy increase in the cellular ROS and Lipid peroxidation (LPO) levels and decrease in Total antioxidant status (TAS) level while pre-treatment with Chr reversed these effects. Dic induction increased the Bax, cytochrome c, cas-3, cas-8 and p53 expression at gene transcription level. Elevated levels of these genes considerably decreased by Chr pre-treatment revealing the defensive effects of Chr. The results obviously presented that exposure of SH-SY5Y with Dic resulted in oxidative stress and apoptosis while pre-treatment of neuron cells with Chr protects the cells against apoptosis triggered by Dic induction.

中文翻译：

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菊花蛋白对双氯芬酸诱导的SH-SY5Y细胞凋亡的神经保护作用。

越来越多的证据表明，活性氧（ROS）可能会严重破坏众多细胞生物分子，从而导致多种神经系统疾病的发展。双氯芬酸（Dic）是最广泛使用的非甾体类抗炎药（NSAID），可通过改变线粒体功能和产生ROS诱导凋亡。菊花（Chr）是一种天然活性成分，存在于许多植物和蜂产品中，并具有很强的神经保护和抗氧化特性。然而，迄今尚未研究Dic诱导的损伤对SH-SY5Y神经元细胞的作用。本研究的目的是研究SH-SY5Y细胞中Chr保护免受Dic引起的氧化损伤的分子机制。Dic对细胞产生明显的毒性，通过用Chr预处理可以逆转这种作用。Dic触发了细胞ROS和脂质过氧化（LPO）水平的显着增加，而总抗氧化剂状态（TAS）的水平下降，而用Chr预处理可以逆转这些作用。Dic诱导在基因转录水平上增加了Bax，细胞色素c，cas-3，cas-8和p53的表达。通过Chr预处理，这些基因的水平显着降低，从而揭示了Chr的防御作用。结果显然表明，SH-SY5Y暴露于Dic会导致氧化应激和细胞凋亡，而用Chr预处理神经元细胞可以保护细胞免受Dic诱导的细胞凋亡。Dic触发了细胞ROS和脂质过氧化（LPO）水平的显着增加，而总抗氧化剂状态（TAS）的水平下降，而用Chr预处理可以逆转这些作用。Dic诱导在基因转录水平上增加了Bax，细胞色素c，cas-3，cas-8和p53的表达。通过Chr预处理，这些基因的水平显着降低，从而揭示了Chr的防御作用。结果显然表明，SH-SY5Y暴露于Dic会导致氧化应激和细胞凋亡，而用Chr预处理神经元细胞可以保护细胞免受Dic诱导的细胞凋亡。Dic触发了细胞ROS和脂质过氧化（LPO）水平的显着增加，而总抗氧化剂状态（TAS）的水平下降，而用Chr预处理可以逆转这些作用。Dic诱导在基因转录水平上增加了Bax，细胞色素c，cas-3，cas-8和p53的表达。通过Chr预处理，这些基因的水平显着降低，从而揭示了Chr的防御作用。结果显然表明，SH-SY5Y暴露于Dic会导致氧化应激和细胞凋亡，而用Chr预处理神经元细胞可以保护细胞免受Dic诱导的细胞凋亡。通过Chr预处理，这些基因的水平显着降低，从而揭示了Chr的防御作用。结果显然表明，SH-SY5Y暴露于Dic会导致氧化应激和细胞凋亡，而用Chr预处理神经元细胞可以保护细胞免受Dic诱导的细胞凋亡。通过Chr预处理，这些基因的水平显着降低，从而揭示了Chr的防御作用。结果显然表明，SH-SY5Y暴露于Dic会导致氧化应激和细胞凋亡，而用Chr预处理神经元细胞可以保护细胞免受Dic诱导的细胞凋亡。