Abstract
Gongjin-dan (GJD) is a multiherbal formula produced from 10 medicinal herbs and has been traditonally used as an oriental medicine to treat cardiovascular diseases, alcoholic hepatitis, mild dementia, and anemia. Additionally, increasing evidence suggests that GJD exerts neuroprotective effects by suppressing inflammation and oxidative stress-induced events to prevent neurological diseases. However, the mechanism by which GJD prevents oxidative stress-induced neuronal injury in a mature neuron remains unknown. Here, we examined the preventive effect and mechanism of GJD on primary cortical neurons exposed to hydrogen peroxide (H2O2). In the neuroprotection signaling pathway, Sirtuin1 is involved in neuroprotective action as a therapeutic target for neurological diseases. After pre-treatment with GJD at three concentrations (10, 25, and 50 µg/mL) and stimulation by H2O2 (30 µM) for 24 h, the influence of GJD on Sirtuin1 activation was assessed using immunocytochemistry, real-time PCR, western blotting, and flow cytometry. GJD effectively ameliorated H2O2-induced neuronal death against oxidative damage through Sirtuin1 activation. In addition, GJD-induced Sirtuin1 activation accelerated elongation of new axons and formation of synapses via increased expression of nerve growth factor and brain-derived neurotrophic factor, as well as regeneration-related genes. Thus, GJD shows potential for preventing neurological diseases via Sirtuin1 activation.
Highlights
Oxidative stress is a pathological hallmark of regenerative failure resulting from an oxidative imbalance between cellular oxidant and antioxidant defense in the nervous system [1,2]
Accumulation of ROS, such as hydrogen peroxide (H2O2), superoxide anion (O2−), and hydroxyl radical (HO·), that exceeds the capacity of the antioxidant system results in neuronal death and functional impairment [4]
The number of live cells was significantly increased following GJD pretreatment, demonstrating that the cells were dose-dependently protected from H2O2 stress (Figure 1C,D)
Summary
Oxidative stress is a pathological hallmark of regenerative failure resulting from an oxidative imbalance between cellular oxidant and antioxidant defense in the nervous system [1,2]. Accumulation of ROS, such as hydrogen peroxide (H2O2), superoxide anion (O2−), and hydroxyl radical (HO·), that exceeds the capacity of the antioxidant system results in neuronal death and functional impairment [4]. Increasing evidence suggests a strong relationship between oxidative stress and neurological diseases, such as Alzheimer’s disease and Parkinson’s disease [5,6]. Oxidative stress contributes to the pathogeneses of secondary damage after traumatic injuries to the spinal cord and brain [7,8]. The regulation of oxidative stress has been suggested for resolving neurological diseases. Natural substances that have been empirically verified as safe and effective have been widely studied
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