ginsenoside-rk1 and Disease-Models--Animal

As the most common sleep disorder, insomnia seriously affects people's everyday lives. Phytochemicals have been shown to have excellent sleep-promoting effects. Therefore, this study was designed to investigate whether Rg5 and Rk1 extracted from ginseng had sleep-promoting effects and to explore their potential mechanisms. The results showed that Rg5 and Rk1 could significantly lessen the locomotor activity of mice and promote the sleep quality index, including increasing the amount of sleep in a pentobarbital sodium experiment with a threshold dose. In parallel, Rg5 and Rk1 could significantly shorten the sleep latency of mice and prolong the sleep time of mice. Furthermore, Rg5 and Rk1 augmented the GABA/Glu ratio, up-regulating the expression of the GABAA receptor and the GABAB receptor, whereas the GABAA receptor antagonist picrotoxin could antagonize the sleep quality of Rg5/Rk1. In addition, 5-HTP, the precursor of 5-HT, could enhance the sleep effect of Rg5 and Rk1 in mice, and both Rg5 and Rk1 could up-regulate the expression of 5-HT1A. These results were also confirmed by the detection of GABA and 5-HT in mouse cecum content. In conclusion, ginsenoside Rg5/Rk1 can exert sedative and hypnotic effects by affecting the GABA nervous system and the serotonin nervous system.

Topics: Animals; Disease Models, Animal; Ginsenosides; Male; Panax; Phytotherapy; Plant Oils; Rats; Rats, Wistar; Receptors, GABA-A; Signal Transduction; Sleep; Sleep Initiation and Maintenance Disorders; Up-Regulation

Neuroblastoma (NB) is the most common childhood cancer, with a very poor prognosis. More than 60% of children with NB die within five years; therefore, a more effective therapy for NB is required. Although ginsenoside has been shown to significantly inhibit the growth of various cancers, the effect of ginsenoside Rk1 on neuroblastoma has not been known yet. Hence, we examined the anticancer effects of highly pure Rk1 on neuroblastoma cell lines. The apoptotic effects of Rk1 on neuroblastoma cells were examined using cell viability assay, flow cytometry and cell staining assay, and the change in gene expression levels were analysed using RT-PCR, western blots, and immunohistochemistry. The metastatic effect of Rk1 was monitored by wound healing assay, invasion and migration with Matrigels. Rk1 inhibited neuroblastoma cell viability dose-dependently. Rk1-induced apoptosis was investigated through nuclear condensation and mitochondrial membrane potential loss, and it showed that Rk1 can induce cell cycle arrest at the G0/G1 phase but also inhibit the metastatic ability of neuroblastoma cells. Moreover, Rk1 (30 mg/kg) injections markedly inhibited xenograft tumor growth. These findings demonstrate that Rk1 might be valuable in the development of anti-cancer agents for neuroblastoma treatment.

Topics: Animals; Apoptosis; Apoptosis Regulatory Proteins; Caspases; Cell Cycle Checkpoints; Cell Line, Tumor; Cell Movement; Cell Proliferation; Cell Survival; Disease Models, Animal; Dose-Response Relationship, Drug; Epithelial-Mesenchymal Transition; Ginsenosides; Humans; Male; Membrane Potential, Mitochondrial; Mice; Molecular Structure; Neuroblastoma; Xenograft Model Antitumor Assays