Nrf2-Keap1 pathway defends organisms against the detrimental effects of oxidative stress, and play pivotal roles in preventing xenobiotic-related toxicity. We designed experiments to explore and verify its role and function under deltamethrin (DM) stress. In experiments, DM was selected as the inducer, and Drosophila Kc cells were treated as the objects. The result showed the oxidative stress of cells proliferated in a very short time after DM treatment, reaching the maximum after one hour of treatment. The experimental data showed Nrf2 could be up-regulated and activated by DM which were manifested by the increase of Nrf2 mRNA, Nrf2 protein in the nucleus and the expression of detoxification enzyme genes. We further tested the activity of all groups, and found the survival rate of cells was basically proportional to the expression of Nrf2. Based on the above experimental results, Keap1 overexpression (K+), Nrf2 overexpression (N+) or interference (N-) cells were used to verified the relationship between Nrf2, cell survival and detoxification enzymes expression. We found the cell survival rate of N+ group was significantly higher than that of other groups and the expression of detoxification enzymes were increased compared to the control group. These results demonstrated that Nrf2 is related to cell detoxification and associated with the tolerance to DM. Our evidence suggested Nrf2 is a potential therapeutic target for oxidative stress and a potential molecular target gene of resistance control.

中文翻译：

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Nrf2-Keap1 通路：果蝇 Kc 细胞中对抗农药迫害的秘密武器

Nrf2-Keap1 通路保护生物体免受氧化应激的不利影响，并在预防外源性相关毒性方面发挥关键作用。我们设计了实验来探索和验证其在溴氰菊酯 (DM) 压力下的作用和功能。实验中选择DM为诱导物，以果蝇Kc细胞为对象。结果显示，DM处理后细胞的氧化应激在极短的时间内增殖，处理1小时后达到最大值。实验数据表明，DM可上调和激活Nrf2，表现为Nrf2 mRNA、细胞核内Nrf2蛋白和解毒酶基因表达增加。我们进一步测试了所有组的活性，发现细胞的存活率与Nrf2的表达基本成正比。基于以上实验结果，分别采用Keap1过表达（K+）、Nrf2过表达（N+）或干扰（N-）细胞来验证Nrf2、细胞存活和解毒酶表达之间的关系。我们发现N+组的细胞存活率明显高于其他组，解毒酶的表达较对照组增加。这些结果表明 Nrf2 与细胞解毒有关，并与对 DM 的耐受性有关。我们的证据表明 Nrf2 是氧化应激的潜在治疗靶点和抗性控制的潜在分子靶基因。细胞存活和解毒酶表达。我们发现N+组的细胞存活率明显高于其他组，解毒酶的表达较对照组增加。这些结果表明 Nrf2 与细胞解毒有关，并与对 DM 的耐受性有关。我们的证据表明 Nrf2 是氧化应激的潜在治疗靶点和抗性控制的潜在分子靶基因。细胞存活和解毒酶表达。我们发现N+组的细胞存活率明显高于其他组，解毒酶的表达较对照组增加。这些结果表明 Nrf2 与细胞解毒有关，并与对 DM 的耐受性有关。我们的证据表明 Nrf2 是氧化应激的潜在治疗靶点和抗性控制的潜在分子靶基因。