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Abstract
Inula britannica var. chinensis (IBC) has been used as a traditional medicinal herb to treat inflammatory diseases. Although its anti-inflammatory and anti-oxidative effects have been reported, whether IBC exerts neuroprotective effects and the related mechanisms in cortical neurons remain unknown. In this study, we investigated the effects of different concentrations of IBC extract (5, 10, and 20 µg/mL) on cortical neurons using a hydrogen peroxide (H2O2)-induced injury model. Our results demonstrate that IBC can effectively enhance neuronal viability under in vitro-modeled reaction oxygen species (ROS)-generating conditions by inhibiting mitochondrial ROS production and increasing adenosine triphosphate level in H2O2-treated neurons. Additionally, we confirmed that neuronal death was attenuated by improving the mitochondrial membrane potential status and regulating the expression of cytochrome c, a protein related to cell death. Furthermore, IBC increased the expression of brain-derived neurotrophic factor and nerve growth factor. Furthermore, IBC inhibited the loss and induced the production of synaptophysin, a major synaptic vesicle protein. This study is the first to demonstrate that IBC exerts its neuroprotective effect by reducing mitochondria-associated oxidative stress and improving mitochondrial dysfunction.
Highlights
Published: 3 March 2021Adenosine triphosphate (ATP), which carries energy for intracellular metabolism, is synthesized in the mitochondria and is mostly used in the cytoplasm [1]
Cortical neurons were treated with Inula britannica var. chinensis (IBC) (0, 5, 10, 20 μg/mL) 24 h after being subjected to
The expression levels of Opa1 were not significantly different between the H2 O2 and IBC groups (Figure 3J). These findings reveal that IBC induced changes in the expression of genes associated with mitochondrial morphology under H2 O2 -induced oxidative stress injury
Summary
Adenosine triphosphate (ATP), which carries energy for intracellular metabolism, is synthesized in the mitochondria and is mostly used in the cytoplasm [1]. The mitochondria play important physiological roles in maintaining cellular homeostasis such as cell growth, cell cycle regulation, production of reactive oxygen species (ROS), and cell death [2,3]. The mitochondria are found in the cytoplasm and along the axon [4]. Most of their mitochondria sustain an injury, and ATP production is either reduced or stopped. When morphological and functional mitochondrial changes occur, most of the oxygen is used to produce ROS.
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