br Conclusions The whole mRNA sequence of

Conclusions The whole mRNA sequence of equine HRG was identified. Consequently, we successfully generated recombinant equine HRG. By the Western blot procedure, blood HRG in horses was detected.
Acknowledgments
Introduction Alzheimer's disease (AD) is a chronic neurological disorder with clinical manifestations of irreversible Omecamtiv mecarbil damage, memory loss and cognitive dysfunction [1]. It may cause aging-related dementia, which affects millions of people worldwide [2]. Although the etiology of AD has not yet been entirely clarified, several pathological changes in AD brains have been identified, including the deposition of amyloid β (Aβ) plagues, abnormal accumulation of neurofibrillary tangles, oxidative stress and extensive neuronal degeneration [[3], [4], [5]]. At present, Donepezil and Rivastigmine as acetylcholinesterase inhibitor are widely used in the treatment of AD. Unfortunately, although remarkable efforts have been devoted for the development of anti-AD drugs, to date, no innovative candidates have successfully gone through phase III clinical trials [6]. Nitric oxide (NO), synthesized from l-arginine by via nitric oxide synthase (NOS)-governed enzyme catalysis, acts as a crucial neurotransmitter and neuromodulator in the mammalian brain [7]. NO mediates a diverse array of physiological processes, and recent evidence suggests the functional role of NO in mediating learning and memory processes [8]. Accumulative studies indicate that NO regulates long-term potentiation (LTP), an indispensable type of synaptic plasticity that contributes to the modulation of learning and memory [9]. In pathogenesis of AD, NO has been implicated to yield both neuroprotective and neurotoxic actions [10], suggesting the maintenance of NO homeostasis is important for preventing the development and progression of AD. Aberrantly enhanced expression of all three isoforms of NOS, including neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial NOS (eNOS), has been detected in neurons and glia of AD brain [11]. It is suggested that Aβ may lead to the overproduction of NO through elevating NOS activity, subsequently induce oxidative damage, and ultimately result in neuronal cell death [12]. Panax ginseng is a widely used traditional Chinese medicine for the treatment of many kind of diseases, for instance cancer, inflammation, cardiovascular disease and neurodegenerative disorder [[13], [14], [15]]. The neuroprotective effects of ginseng have long been observed, and recent study implicates the therapeutic potential of ginseng for the treatment of various central nervous system disorders. Ginsenoside Rg1 has been demonstrated to reduce β-secretase activity and calcium influx [16]. Rb1 has been found to have a regulatory effect in PI3K/AKT pathway, thereby reducing the phosphorylation of Tau protein in the brain. In our previous report [17]. We found that the aqueous extract isolated from ginseng prevented against scopolamine-induced memory deficit in rats [18]. Nevertheless, the potential activity of ginseng extracts in AD-like neuronal injury and rodent memory function remains unclear. Aβ25–35, the neurotoxic domain of full-length Aβ, has been widely used to induce AD-like neuronal cell injury both in vitro and in vivo [19,20]. There is increasing evidence that Aβ25–35 induces cell apoptosis through stimulating ROS-NO pathway [21]. In this study, AD rats were prepared by the injection of Aβ25–35 into the hippocampus. In addition, Aβ25–35 was used to induce AD-like neuronal injury in the human neuroblastoma SH-SY5Y cell line. Therefore, we hypothesized that glycoprotein derived from the aqueous extract of ginseng reduce Aβ25–35-induced apoptosis. We discussed the protection of glycoprotein by detecting the behavioral experiment, ratio of apoptosis cells, cell cycle and NO/NOS-release. Our findings provide valuable insights into understanding the preliminary mechanism of glycoprotein of ginseng induced anti-AD activities.