Hong Jin Young, Kim Hyunseong, Jeon Wan-Jin, Baek Seungho, Ha In-Hyuk
Jaseng Spine and Joint Research Institute, Jaseng Medical Foundation, Seoul 135-896, Korea.
College of Korean Medicine, Dongguk University, 32 Dongguk-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do 10326, Korea.
Antioxidants (Basel). 2020 Jun 23;9(6):548. doi: 10.3390/antiox9060548.
Oxidative stress plays a key role in the pathogenesis of several diseases, including neurodegenerative diseases. Recent studies have reported that mitochondrial dysfunction is a leading cause of the overproduction of reactive oxygen species and oxidative stress. Mitochondrial changes play an important role in preventing oxidative stress. However, there is a lack of experimental evidence supporting this hypothesis. CELAK (TQC) extract is a plant from China belonging to the thymus species, which can mediate the inflammatory response and prevent cell damage through its antioxidant activities. This study examines whether TQC can scavenge excess ROS originating from the mitochondria in RAW 264.7 macrophages. We used lipopolysaccharide (LPS) to induce inflammation and oxidative stress in RAW 264.7 macrophages and performed an immunocytochemistry dot blot of 8-hydroxy-2'-deoxyguanosine (8-OHdG) and real-time PCR to analyze the expression levels of genes involved in mitochondrial biogenesis and oxidative metabolism. TQC was found to significantly reduce the intensity of immunostained MitoSOX and 8-OHdG levels in the total genomic DNA within the mitochondria in RAW 264.7 macrophages. The HO-1 and Nrf2 mRNA levels were also significantly increased in the TQC groups. Therefore, we verified that TQC improves mitochondrial function and attenuates oxidative stress induced by LPS. Our results can provide reference for the effect of TQC to develop new therapeutic strategies for various diseases.
氧化应激在包括神经退行性疾病在内的多种疾病的发病机制中起关键作用。最近的研究报告称，线粒体功能障碍是活性氧过度产生和氧化应激的主要原因。线粒体变化在预防氧化应激中起重要作用。然而，缺乏支持这一假设的实验证据。CELAK（TQC）提取物是一种来自中国的属于百里香属的植物，它可以通过其抗氧化活性介导炎症反应并防止细胞损伤。本研究探讨TQC是否能清除RAW 264.7巨噬细胞中线粒体产生的过量活性氧。我们使用脂多糖（LPS）诱导RAW 264.7巨噬细胞发生炎症和氧化应激，并进行8-羟基-2'-脱氧鸟苷（8-OHdG）的免疫细胞化学斑点印迹和实时PCR，以分析参与线粒体生物发生和氧化代谢的基因的表达水平。结果发现，TQC可显著降低RAW 264.7巨噬细胞线粒体中免疫染色的MitoSOX强度和总基因组DNA中的8-OHdG水平。TQC组中HO-1和Nrf2 mRNA水平也显著升高。因此，我们证实TQC可改善线粒体功能并减轻LPS诱导的氧化应激。我们的结果可为TQC的作用提供参考，以开发针对各种疾病的新治疗策略。
