Abstract

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. Thymus quinquecostatus 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.

Highlights

  • An excessive increase in intracellular reactive oxygen species creates oxidative stress and prevents cells from functioning normally, inducing cell death

  • To examine the effects of Thymus quinquecostatus CELAK (TQC) on antioxidants in LPS-activated RAW 264.7 macrophages 24 h after treatment, we evaluated the production of NO using the Griess assay

  • We confirmed that TQC restores reduced mitochondrial function, which was induced by LPS, and facilitates the sufficient supply of oxygen needed for energy metabolism, thereby aiding in adenosine triphosphate (ATP) synthesis

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Summary

Introduction

An excessive increase in intracellular reactive oxygen species creates oxidative stress and prevents cells from functioning normally, inducing cell death. Mitochondria are the key organelles that produce ROS, and, in normal mitochondria, 90–95% of the total oxygen is used to produce adenosine triphosphate (ATP), whereas 1–2% is converted to ROS during cellular metabolism [4]. These ROS, the generation of which is inevitable, play a role in the destruction of foreign invaders, such as bacteria or viruses, and in hormone regulation. Recent studies have suggested that the excessive release of Antioxidants 2020, 9, 548; doi:10.3390/antiox9060548 www.mdpi.com/journal/antioxidants

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