Chlorpyrifos (CPF), an insecticide, induces pro-oxidant, pro-inflammatory, and pro-apoptotic effects in animal cells. Contamination with CPF occurs not only in farms, since CPF is found in the food consumed in homes. Recently, it was demonstrated that CPF affects the mitochondria, inhibiting components of the electron transfer chain (ETC), causing loss of mitochondrial membrane potential (MMP), and reducing the synthesis of adenosine triphosphate (ATP) by the Complex V. Pinocembrin (PB) is found in propolis and exhibits antioxidant, anti-inflammatory, and anti-apoptotic effects in mammalian cells. PB is a potent inducer of the nuclear factor erythroid 2-related factor 2 (Nrf2), which is a major transcription factor controlling the expression of heme oxygease-1 (HO-1), among others. In the present work, we investigated whether PB would be able to prevent the mitochondrial and immune dysfunctions in the human neuroblastoma SH-SY5Y cells exposed to CPF. PB was tested at 1–25 µM for 4 h before the administration of CPF at 100 µM for additional 24 h. We found that PB prevented the CPF-induced inhibition of ETC, loss of MMP, and decline in the ATP synthesis. PB also promoted anti-inflammatory actions in this experimental model. Silencing of Nrf2 or inhibition of HO-1 suppressed the PB-induced effects in the CPF-challenged cells. Thus, PB promoted beneficial effects by a mechanism dependent on the Nrf2/HO-1/CO + BR axis in the CPF-treated cells.

毒死蜱 (CPF) 是一种杀虫剂，可在动物细胞中诱导促氧化、促炎和促凋亡作用。CPF 污染不仅发生在农场，因为 CPF 存在于家庭消费的食物中。最近，证明CPF影响线粒体，抑制电子传递链（ETC）的成分，导致线粒体膜电位（MMP）的丧失，并减少复合物V. Pinocembrin（PB）合成三磷酸腺苷（ATP） ) 存在于蜂胶中，在哺乳动物细胞中表现出抗氧化、抗炎和抗凋亡作用。PB 是核因子红细胞 2 相关因子 2 (Nrf2) 的有效诱导剂，Nrf2 是控制血红素氧化酶 1 (HO-1) 等表达的主要转录因子。在目前的工作中，我们研究了 PB 是否能够预防暴露于 CPF 的人类神经母细胞瘤 SH-SY5Y 细胞的线粒体和免疫功能障碍。PB 在 1-25 µM 下测试 4 小时，然后再以 100 µM 的 CPF 给药 24 小时。我们发现 PB 阻止了 CPF 诱导的 ETC 抑制、MMP 的丢失和 ATP 合成的下降。在这个实验模型中，PB 还促进了抗炎作用。Nrf2 的沉默或 HO-1 的抑制抑制了 PB 诱导的 CPF 攻击细胞中的作用。因此，PB 通过依赖于 CPF 处理细胞中 Nrf2/HO-1/CO + BR 轴的机制来促进有益效果。我们发现 PB 阻止了 CPF 诱导的 ETC 抑制、MMP 的丢失和 ATP 合成的下降。在这个实验模型中，PB 还促进了抗炎作用。Nrf2 的沉默或 HO-1 的抑制抑制了 PB 诱导的 CPF 攻击细胞中的作用。因此，PB 通过依赖于 CPF 处理细胞中 Nrf2/HO-1/CO + BR 轴的机制来促进有益效果。我们发现 PB 阻止了 CPF 诱导的 ETC 抑制、MMP 的丢失和 ATP 合成的下降。在这个实验模型中，PB 还促进了抗炎作用。Nrf2 的沉默或 HO-1 的抑制抑制了 PB 诱导的 CPF 攻击细胞中的作用。因此，PB 通过依赖于 CPF 处理细胞中 Nrf2/HO-1/CO + BR 轴的机制来促进有益效果。