Emodin (EM; 1,3,8-trihydroxy-6-methylanthracene-9,10-dione; C₁₅H₁₀O₅) is an anthraquinone and exerts cytoprotective effects, as observed in both in vitro and in vivo experimental models. Mitochondrial dysfunction induced by reactive species plays a central role in the onset and progression of different human diseases. Thus, we have tested here whether a pretreatment (for 4 h) with EM (at 40 µM) would be able to promote mitochondrial protection in the human neuroblastoma SH-SY5Y cells exposed to the pro-oxidant agent hydrogen peroxide (H₂O₂). We found that the pretreatment with EM suppressed the effects of H₂O₂ on the activity of the mitochondrial complexes I and V, as well as on the production of adenosine triphosphate (ATP) and on the mitochondrial membrane potential (MMP). EM also prevented the H₂O₂-induced collapse in the tricarboxylic acid cycle (TCA) function. An anti-inflammatory role for EM was also observed in this experimental model, since this anthraquinone decreased the secretion of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) by the H₂O₂-challenged cells. Inhibition of the adenosine monophosphate-activated protein kinase (AMPK) or silencing of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) abolished the protection induced by EM in the H₂O₂-treated cells. Therefore, EM prevented the H₂O₂-induced mitochondrial dysfunction and pro-inflammatory state in the SH-SY5Y cells by an AMPK/Nrf2-dependent manner.

大黄素（EM；1,3,8-trihydroxy-6-methylanthracene-9,10-dione；C ₁₅ H ₁₀ O ₅）是一种蒽醌并发挥细胞保护作用，如在体外和体内实验模型中所观察到的。由活性物质诱导的线粒体功能障碍在不同人类疾病的发生和发展中起着核心作用。因此，我们在这里测试了用 EM（40 µM）预处理（4 小时）是否能够促进暴露于促氧化剂过氧化氢（H ₂ O ₂）。我们发现 EM 预处理抑制了 H ₂ O ₂线粒体复合物 I 和 V 的活性，以及​​三磷酸腺苷 (ATP) 的产生和线粒体膜电位 (MMP)。EM 还阻止了 H ₂ O ₂诱导的三羧酸循环 (TCA) 功能崩溃。在该实验模型中还观察到 EM 的抗炎作用，因为这种蒽醌减少了 H ₂ O ₂攻击细胞的白细胞介素-1β (IL-1β) 和肿瘤坏死因子-α (TNF-α) 的分泌. 抑制一磷酸腺苷活化蛋白激酶 (AMPK) 或沉默转录因子核因子类红细胞 2 相关因子 2 (Nrf2) 消除了 EM 在 H ₂ O _{2 中}诱导的保护-处理过的细胞。因此，EM通过AMPK/Nrf2依赖性方式防止H ₂ O ₂诱导的SH-SY5Y细胞中的线粒体功能障碍和促炎状态。