IRCCS Centro Neurolesi "Bonino Pulejo", 98124 Messina, Italy.
Department of Pharmaceutical Sciences, University of Eastern Piedmont "Amedeo Avogadro", 28100 Novara, Italy.
Int J Mol Sci. 2018 Jul 8;19(7):1992. doi: 10.3390/ijms19071992.
Inflammation and oxidative stress play main roles in neurodegeneration. Interestingly, different natural compounds may be able to exert neuroprotective actions against inflammation and oxidative stress, protecting from neuronal cell loss. Among these natural sources, represents a reservoir of compounds exerting beneficial properties, including cannabigerol (CBG), whose antioxidant properties have already been demonstrated in macrophages. Here, we aimed to evaluate the ability of CBG to protect NSC-34 motor neurons against the toxicity induced from the medium of LPS-stimulated RAW 264.7 macrophages. Using MTT assay, we observed that CBG pre-treatment was able to reduce the loss of cell viability induced by the medium of LPS-stimulated macrophages in NSC-34 cells. Indeed, CBG pre-treatment inhibited apoptosis, as shown by the reduction of caspase 3 activation and Bax expression, while Bcl-2 levels increased. Furthermore, CBG pre-treatment counteracted not only inflammation, as demonstrated by the reduction of IL-1β, TNF-α, IFN-γ and PPARγ protein levels assessed by immunocytochemistry, but also oxidative stress in NSC-34 cells treated with the medium of LPS-stimulated RAW 264.7. Indeed, immunocytochemistry showed that CBG pre-treatment reduced nitrotyrosine, SOD1 and iNOS protein levels and restored Nrf-2 levels. All together, these results indicated the neuroprotective effects of CBG, that may be a potential treatment against neuroinflammation and oxidative stress.
炎症和氧化应激在神经退行性变中起主要作用。有趣的是，不同的天然化合物可能能够发挥神经保护作用，对抗炎症和氧化应激，从而防止神经元细胞丢失。在这些天然来源中，大麻代表了发挥有益特性的化合物的宝库，包括大麻素二醇（CBG），其抗氧化特性已在巨噬细胞中得到证实。在这里，我们旨在评估 CBG 保护 NSC-34 运动神经元免受 LPS 刺激的 RAW 264.7 巨噬细胞培养基毒性的能力。通过 MTT 测定，我们观察到 CBG 预处理能够减少 LPS 刺激的巨噬细胞培养基诱导的 NSC-34 细胞活力丧失。事实上，CBG 预处理抑制了细胞凋亡，这表现为 caspase 3 激活和 Bax 表达减少，而 Bcl-2 水平增加。此外，CBG 预处理不仅对抗了炎症，如通过免疫细胞化学评估的 IL-1β、TNF-α、IFN-γ和 PPARγ蛋白水平的降低所示，而且还对抗了 LPS 刺激的 RAW 264.7 巨噬细胞培养基处理的 NSC-34 细胞中的氧化应激。事实上，免疫细胞化学显示 CBG 预处理降低了硝基酪氨酸、SOD1 和 iNOS 蛋白水平，并恢复了 Nrf-2 水平。所有这些结果表明了 CBG 的神经保护作用，它可能是一种针对神经炎症和氧化应激的潜在治疗方法。
