Abstract
BackgroundWedelia chinensis is traditionally used as a hepatoprotective herb in Taiwan. The aim of this study was to evaluate the neuroprotective potential of W. chinensis.MethodsAn ethyl acetate extract of W. chinensis (EAW) was prepared and analyzed by HPLC. The neuroprotective potential of EAW was assessed by tert-butylhydroperoxide (t-BHP)-induced damage in PC12 cells and D-galactose-induced damage in mouse cortex.ResultsEAW exhibited potent radical scavenging property and highly contained luteolin and wedelolactone. EAW decreased t-BHP-induced reactive oxygen species (ROS) accumulation, cytotoxicity and apoptosis in PC12 cells. EAW and its major constituents blocked t-BHP-induced cytochrome C release and Bcl-2 family protein ratio change. EAW and its major constituents increased the endogenous antioxidant capacity evaluated by the binding activity assay of nuclear factor E2-related factor 2 (Nrf2) to antioxidant response element (ARE) and nuclear translocation of Nrf2 respectively in PC12 cells. Finally, EAW inhibited D-galactose-induced lipid peroxidation, apoptosis and neuron loss in the cerebral cortex of mice.ConclusionThese results demonstrate that W. chinensis has neuroprotective potential through blocking oxidative stress-induced damage and that luteolin and wedelolactone contribute to the protective action.
Highlights
Wedelia chinensis is traditionally used as a hepatoprotective herb in Taiwan
The brain is especially vulnerable to oxidative stress compared to other organs because it exhibits lower antioxidant enzyme activity and contains an abundance of unsaturated fatty acids, which are the targets of lipid peroxidation
Ethanol extract of W. chinensis exhibited free radical scavenging activity, and after solvent partition, it showed EAW increased the potency of free radical scavenging activity, with 10 μg/mL of EAW quenching ~50% of free radicals (Figure 1A)
Summary
Wedelia chinensis is traditionally used as a hepatoprotective herb in Taiwan. The aim of this study was to evaluate the neuroprotective potential of W. chinensis. Apart from quenching free radicals, antioxidants may Tertiary butyl hydroperoxide (t-BHP), a simple lipophilic alkyl hydroperoxide, has been reported to induce dosedependent oxidative stress and damage in brain cells [2]. The alkoxyl and alkyl radicals derived from t-BHP are a species that produce cell damage [3,4]. T-BHP is a useful inducer for investigating the effectiveness of various neuroprotection products against oxidative stress. High concentrations are converted into aldose and hydroperoxide by galactose oxidase, resulting in the generation of ROS in the brain [6,7], which can affect bimolecules including protein, DNA and lipids and which may lead to consecutive functional disturbance and cell death. Treatment of animals with D-galactose may serve as a useful model for studying the effect of neuroprotective agents
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