Objective Our previous in vivo study found that resveratrol (Res), which is a phytoalexin, attenuated 6-hydroxydopamine (6-OHDA)-induced motor dysfunction by activating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway in rats. Therefore, we further explored the protective effect of Res on 6-OHDA-induced damage to PC12 cells in vitro with respect to the PI3K/Akt signaling pathway. Methods We incubated PC12 cells with 75 μM 6-OHDA for 24 h, and Res was then added at a final concentration of 25 μM; the protective effect was examined via MTT and lactate dehydrogenase (LDH) assays. In addition, the PI3K inhibitor LY294002 was used to investigate the potential mechanism. JC-1 staining was used to detect the mitochondrial membrane potential (MMP), and western blotting (WB) was used to detect the phosphorylation of Akt-Ser473. Results Compared with that in the control, the cell viability, total superoxide dismutase (SOD) activity, MMP, and p-Akt-Ser473 level of 6-OHDA-treated PC12 cells were significantly decreased, while the leakage rate of LDH was increased. And after treatment with 25 μM Res, the cell viability, total SOD activity, MMP, and p-Akt-Ser473 level of 6-OHDA-treated PC12 cells were significantly increased compared with those of the control cells, while the leakage rate of LDH was decreased. These effects of Res were antagonized by LY294002. Conclusions Res ameliorates 6-OHDA-induced damage to PC12 cells via activation of the PI3K/Akt signaling pathway.

中文翻译：

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白藜芦醇通过PI3K / Akt对抗6-OHDA诱导的PC12细胞损伤

目的我们以前的体内研究发现，植物白藜芦醇（Res）通过激活磷脂酰肌醇3-激酶/蛋白激酶B（PI3K / Akt）信号转导通路，减轻了6-羟多巴胺（6-OHDA）引起的运动功能障碍。大鼠。因此，我们进一步探讨了Res在PI3K / Akt信号通路方面对6-OHDA诱导的PC12细胞损伤的保护作用。方法我们将PC12细胞与75μM6-OHDA孵育24小时，然后以25μM的终浓度添加Res；通过MTT和乳酸脱氢酶（LDH）测定法检查保护作用。此外，PI3K抑制剂LY294002用于研究潜在的机制。JC-1染色用于检测线粒体膜电位（MMP），免疫印迹法（WB）检测Akt-Ser473的磷酸化。结果与对照组相比，经6-OHDA处理的PC12细胞的细胞活力，总超氧化物歧化酶（SOD）活性，MMP和p-Akt-Ser473水平显着降低，而LDH的漏出率增加。用25μMRes处理后，6-OHDA处理的PC12细胞的细胞活力，总SOD活性，MMP和p-Akt-Ser473水平与对照细胞相比显着提高，而LDH的漏出率减少了。Res的这些作用被LY294002拮抗。结论Res通过激活PI3K / Akt信号通路改善了6-OHDA诱导的PC12细胞损伤。6-OHDA处理的PC12细胞的p-Akt-Ser473和p-Akt-Ser473的水平显着降低，而LDH的泄漏率却增加了。用25μMRes处理后，6-OHDA处理的PC12细胞的细胞活力，总SOD活性，MMP和p-Akt-Ser473水平与对照细胞相比明显增加，而LDH的漏出率减少了。Res的这些作用被LY294002拮抗。结论Res通过激活PI3K / Akt信号通路改善了6-OHDA诱导的PC12细胞损伤。6-OHDA处理的PC12细胞的p-Akt-Ser473和p-Akt-Ser473的水平显着降低，而LDH的泄漏率却增加了。用25μMRes处理后，6-OHDA处理的PC12细胞的细胞活力，总SOD活性，MMP和p-Akt-Ser473水平与对照细胞相比明显增加，而LDH的漏出率减少了。Res的这些作用被LY294002拮抗。结论Res通过激活PI3K / Akt信号通路改善了6-OHDA诱导的PC12细胞损伤。LDH的泄漏率降低。Res的这些作用被LY294002拮抗。结论Res通过激活PI3K / Akt信号通路改善了6-OHDA诱导的PC12细胞损伤。LDH的泄漏率降低。Res的这些作用被LY294002拮抗。结论Res通过激活PI3K / Akt信号通路改善了6-OHDA诱导的PC12细胞损伤。