The present study explored the neuroprotective effect of Coeloglossum viride var. bracteatum extract (CE) against oxidative stress in rat cortical neurons. The results demonstrated that administration of CE inhibited hydrogen peroxide-induced neurotoxicity tested by MTT, LDH release, and TUNEL assays. We further found that CE inhibited the activation of caspase-3 (Csp3) induced by hydrogen peroxide. Moreover, CE was found to reverse the hydrogen peroxide-induced downregulation of active AKT and Bcl-2. We then showed that the neuroprotective effect of CE was blocked by adding the AKT inhibitor, Ly294002. Thus, our data strongly indicated that CE played a neuroprotective role against oxidative stress-induced neurotoxicity. 1. Introduction Coeloglossum viride var. bracteatum extract (CE) is extracted from a plant called Coeloglossum viride var. bracteatum, an orchidaceae family plant. CE is widely used as a traditional Chinese medicine in the Northwest of China, especially in Tibet, Qinghai, Gansu Inner Mongolia, and Shanxi provinces [1]. It has been described as a traditional Chinese medicine; CE increases body fluid production and vital energy is beneficiary to memory and tranquilization [1]. In 2004, CE has been identified as a mixture of four compounds [2]. More recently, CE has been shown to rescue learning and memory deficit induced by scopolamine in rodents [3]. Alzheimer’s Disease (AD) is a progressive neurodegenerative disease characterized by extracellular senile plaques composed of amyloid beta and intracellular neurofibrillary tangles (NFTs) [4]. Neuronal loss in AD is thought to be contributed by amyloid beta toxicity [5], and growing evidence suggests that the amyloid beta toxicity is mediated by oxidative damage in neurons [4]. Numerous studies suggested that oxidative stress plays a major role in the pathogenesis of AD. It has been observed that oxidative stress is increased in brains from patients with AD [6]. Moreover, reduction of antioxidant enzyme activity including superoxide dismutase (SOD) and catalase has been reported in brains from patients with AD [7, 8]. In addition, deficiency of superoxide dismutase D1 (Sod1) in a mouse model of AD resulted in accelerated amyloid beta plaque formation and memory deficit, and the phenomena were mediated by oxidative damage [9]. Interestingly, a recent study found that an antioxidant MitoQ blocked increased oxidative stress, increased amyloid beta plaque formation, and elevated caspase activity and synaptic loss in an animal model of AD [10]. Thus oxidative stress is a promising therapeutic
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