liriodendrin--1r-(1alpha-3abeta-4beta-6aalpha)-isomer and Disease-Models--Animal

This research investigated the effects of eleutheroside E (EE) on the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease cell model and its mechanism. Methods: To create a cell model of Parkinson's disease, MPTP (2500 μmol/L) was administered to rat adrenal pheochromocytoma cells (PC-12) to produce an MPTP group. Selegiline (50 μmol/L) and MPTP had been administered to the positive group beforehand. The eleutheroside E group was divided into low-, medium-, and high-concentration groups, in which the cells were pretreated with eleutheroside E at concentrations of 100 μmol/L, 300 μmol/L, and 500 μmol/L. Next, MPTP was added to the cells separately. The CCK-8 method was used to measure the cell survival rate. Apart from the CCK-8 method, mitochondrial membrane potential detection, cell reactive oxygen species (ROS) detection, and other methods were also adopted to verify the effect of low, medium, and high concentrations of eleutheroside E on the MPTP-induced cell model. Western blot analysis was used to detect changes in the expression of intracellular proteins CytC, Nrf2, and NQO1 to clarify the mechanism. The results are as follows. Compared with the MPTP group, the survival rates of cells at low, medium, and high concentrations of eleutheroside E all increased. The mitochondrial membrane potential at medium and high concentrations of eleutheroside E increased. The ROS levels at medium and high concentrations of eleutheroside E decreased. Moreover, the apoptosis rate decreased and the expression levels of the intracellular proteins CytC, Nrf2, and NQO1 were upregulated. Conclusion: Eleutheroside E can improve the MPTP-induced apoptosis of PC-12 cells by increasing the mitochondrial membrane potential and reducing the level of intracellular reactive oxygen species (ROS). Moreover, the apoptosis of cells is regulated by the expression of CytC, Nrf2, and NQO1 proteins.

Topics: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Animals; Disease Models, Animal; Mice; Mice, Inbred C57BL; NF-E2-Related Factor 2; Parkinson Disease; Rats; Reactive Oxygen Species

Topics: Animals; Brain Injuries; Computational Biology; Disease Models, Animal; Eleutherococcus; Gene Expression Profiling; Gene Ontology; Gene Regulatory Networks; Glucosides; Lignans; Male; Mice; Neuroprotective Agents; Phenylpropionates; Phytochemicals; Plant Extracts; Polysaccharides; Proteome; Proteomics; Radiation Injuries, Experimental

Glomerular hypertrophy and extracellular matrix accumulation are early features of diabetic nephropathy (DN). High glucose-induced oxidative stress is implicated in the etiology of DN. This study aims to investigate the effect of eleutheroside E (EE) on high glucose mediated rat mesangial cells (MCs) proliferation and monocyte chemoattractant protein-1 (MCP-1) expression and the underlying mechanism. MCs proliferation was assessed by MTT assay. Reactive oxygen species (ROS) level and MCP-1 expression were evaluated by ELISA kit. The protein expression of p47, NF-κB p65, p-NF-κB p65, IκBα, p-IκBα, IKKβ and p-IKKβ were determined by Western blot. The results showed that treatment with EE markedly attenuated high glucose induced MCs proliferation and in a dose-dependent manner. Intervention with EE also significantly blocked high glucose induced intracellular ROS production by decreasing NADPH oxidase activity. Meanwhile, EE administration could effectively alleviate the high glucose-stimulated activation of NF-κB, the degradation of IκBα and the expression of MCP-1. These results demonstrate that high glucose enhances MCs proliferation and MCP-1 expression by activating the ROS/NF-κB pathway and can be inhibited by EE. Our findings provide a new perspective for the clinical treatment of DN.

Topics: Animals; Cell Proliferation; Chemokine CCL2; Diabetic Nephropathies; Disease Models, Animal; Gene Expression Regulation; Glucose; Glucosides; Humans; I-kappa B Proteins; Lignans; Mesangial Cells; NADPH Oxidases; NF-kappa B; NF-KappaB Inhibitor alpha; Rats; Reactive Oxygen Species; Signal Transduction; Transcription Factor RelA

Eleutheroside E (EE), a principal component of Eleutherococcus senticosus, has been reported to have anti-inflammatory and protective effects in ischemia heart etc. However, whether it can mitigate behavioral alterations induced by sleep deprivation, has not yet been elucidated. Numerous studies have demonstrated that memory deficits induced by sleep deprivation in experimental animals can be used as a model of behavioral alterations. The present study investigated the effect of EE, on cognitive performances and biochemical parameters of sleep-deprived mice. Animals were repeatedly treated with saline, 10 or 50mg/kg EE and sleep-deprived for 72 h by the multiple platform method. Briefly, groups of 5-6 mice were placed in water tanks (45 × 34 × 17 cm), containing 12 platforms (3 cm in diameter) each, surrounded by water up to 1cm beneath the surface or kept in their home cage. After sleep deprivation, mice showed significant behavioral impairment as evident by reduced latency entering into a dark chamber, locomotion and correctly rate in Y maze, and increased monoamines in hippocampus. However, repeated treatment with EE restored these behavioral and biochemical alterations in mice. In conclusion, the beneficial effect of EE may provide an effective and powerful strategy to alleviate behavioral alterations induced by sleep deprivation.

Topics: Animals; Antioxidants; Avoidance Learning; Behavior, Animal; Body Weight; Disease Models, Animal; Dopamine; Glucosides; Glutathione; Hippocampus; Lignans; Locomotion; Male; Malondialdehyde; Maze Learning; Mice; Mice, Inbred ICR; Neurotransmitter Agents; Serotonin; Sleep Deprivation; Stress, Psychological; Time Factors