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Project description:RNA-sequencing of DMSO or Ginsenoside Rb1-treated Rat BMSCs
| PRJNA856660 | ENA
Project description:To understand the effect of DMSO in preimplantation embryos, we have treated mouse 1 cell zygotes with DMSO and found that DMSO treatment caused 2 or 4 cell embryonic arrest and altered the acetylation levels of mouse preimplantation embryos To illustrate the mechanism of DMSO in mouse preimplantation embryos, fertilized zygotes have been treated with 2% of DMSO and then performed RNA-seq analyses. Differentially expressed genes were identified using DESeq2 after adjustment for false discovery rate (FDR q value < 0.05). Gene Set Enrichment Analysis (GSEA) was also performed to identify biological pathways significantly modulated by DMSO. Raw and processed RNA-seq data were deposited and made publicly available on the Gene Expression Omnibus (GEO; GSE124598). The data presented in this article are related to the research paper entitled "DMSO impairs the transcriptional program for maternal-to-embryonic transition by altering histone acetylation", available in Biomaterials [1].
| S-EPMC6940686 | biostudies-literature
Project description:Parkinson's disease (PD) is a common neurodegenerative disease, featured by motor deficits and non-motor symptoms such as cognitive impairment, and malfunction of gamma-aminobutyric acid (GABA) mediated inhibitory transmission plays an important role in PD pathogenesis. The ginsenoside Rb1 molecule, a major constituent of the extract from the Ginseng root, has been demonstrated to ameliorate motor deficits and prevent dopaminergic neuron death in PD. However, whether Rb1 can regulate GABAergic transmission in PD-associated deficits and its underlying mechanisms are still unclear. In this study, we explored the effects of Rb1 on the GABAergic synaptic transmission in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. We demonstrated that Rb1 can bind with GABAARα1 and increase its expression in the SH-SY5Y cells and in the prefrontal cortex (PFC) of MPTP model in vitro and in vivo. Furthermore, Rb1 can promote prefrontal cortical GABA level and GABAergic transmission in MPTP-treated mice. We also revealed that Rb1 may suppress presynaptic GABABR1 to enhance GABA release and GABAA receptor-mediated inhibitory transmission. In addition, Rb1 attenuated MPTP-induced dysfunctional gait dynamic and cognitive impairment, and this neuroprotective mechanism possibly involved regulating prefrontal cortical GABAergic transmission. Thus, Rb1 may serve as a potential drug candidate for the treatment of PD.
| S-EPMC6682523 | biostudies-literature
Project description:Alzheimer's disease (AD) is the most common form of dementia and lacks disease-altering treatments. Ginsenoside Rb1 (GsRb1), the key active compounds of ginsenoside found in ginseng. The present study aimed to determine whether GsRb1 could prevent cognitive deficit and take neuroprotective effects in Aβ1-40-induced rat model through apoptotic signaling pathway. Injection of soluble Aβ1-40 into the hippocampus caused impairment in learning and memory. Daily administration of Rb1 (12.5, 25, and 50 mg/kg, i.p.) for 14 consecutive days. All rats were tested for their capabilities of spatial navigation and memorization by Morris water maze. Apoptosis was tested using TUNEL staining in hippocampus neuronal cells. RT-PCR, immunohistochemical staining and western blotting were employed to confirm the expressions of Bcl-2, Bax and Cleaved Caspase-3. The results showed that Rb1 administration could prevent cognitive deficit, and significantly decreased the levels of Bax and Cleaved Caspase-3 meanwhile up regulation the level of Bcl-2 in the hippocampus. We suggest that GsRb1 may be effective for preventing or slowing the development of Alzheimer's disease, which improving cognitive and memory functions by inhibiting the levels of pro-apoptosis mediators and improving the levels of anti-apoptosis mediators in the rat brain.
| S-EPMC5883120 | biostudies-literature
Project description:Ginsenoside Rg1 and Rb1 are the major ingredients in two medicines called QiShengLi (Z20027165) and QiShengJing (Z20027164) approved by China. These ingredients are believed to mitigate forgetfulness. Numerous studies have confirmed that GRg1 and GRb1 offer protection against Alzheimer's disease (AD), and our morris water maze (MWM) experiment also indicated that GRg1 and GRb1 may attenuate memory deficits in the 7-month-old SAMP8 mice; however, comprehensive understanding of their roles in AD remains limited. This study systematically explored the mechanism at the genome level of the anti-AD effects of GRg1 and GRb1 in a senescence-accelerated mouse prone 8 (SAMP8) model through deep RNA sequencing. A total of 74,885 mRNA transcripts were obtained. Expression analysis showed that 1,780 mRNA transcripts were differentially expressed in SAMP8 mice compared with the SAMP8+GRg1 mice. Moreover, 1,066 significantly dysregulated mRNA transcripts were identified between SAMP8 and SAMP8+GRb1 mice. Analyses according to gene ontology and the Kyoto Encyclopedia of Genes and Genomes revealed that oral administration of GRg1 and GRb1 improved the learning performance of the SAMP8 mouse model from various aspects, such as nervous system development and mitogen-activated protein kinase signaling pathway. The most probable AD-related transcriptional responses after medication were predicted and discussed in detail. This study is the first to provide a systematic dissection of mRNA profiling in SAMP8 mouse brain in response to GRg1 and GRb1 treatment. We explained their efficacy thoroughly from the source (gene-level explanation). The findings serve as a theoretical basis for the exploration of GRg1 and GRb1 as functional drugs with anti-AD activity.
| S-EPMC5326756 | biostudies-literature
Project description:Ginsenoside Rb1 is one of the main active principles in traditional herb ginseng and has been reported to have a wide variety of neuroprotective effects. Endoplasmic reticulum (ER) stress has been implicated in neurodegenerative diseases, so the present study aimed to observe the effects of ginsenoside Rb1 on ER stress signaling pathways in high glucose-treated hippocampal neurons. The results from MTT, TUNEL labeling and Annexin V-FITC/PI/Hoechst assays showed that incubating neurons with 50 mM high glucose for 72 h decreased cell viability and increased the number of apoptotic cells whereas treating neurons with 1 μM Rb1 for 72 h protected the neurons against high glucose-induced cell damage. Further molecular mechanism study demonstrated that Rb1 suppressed the activation of ER stress-associated proteins including protein kinase RNA (PKR)-like ER kinase (PERK) and C/EBP homology protein (CHOP) and downregulation of Bcl-2 induced by high glucose. Moreover, Rb1 inhibited both the elevation of intracellular reactive oxygen species (ROS) and the disruption of mitochondrial membrane potential induced by high glucose. In addition, the high glucose-induced cell apoptosis, activation of ER stress, ROS accumulation and mitochondrial dysfunction can also be attenuated by the inhibitor of ER stress 4-phenylbutyric acid (4-PBA) and anti-oxidant N-acetylcysteine(NAC). In conclusion, these results suggest that Rb1 may protect neurons against high glucose-induced cell injury through inhibiting CHOP signaling pathway as well as oxidative stress and mitochondrial dysfunction.
| S-EPMC3815219 | biostudies-literature
Project description: Not available
| S-EPMC10945261 | biostudies-literature
Project description:Mitochondrial damage caused by oxidative stress and energy deficiency induced by focal ischemia and hypoxia are important factors that aggravate diseases. Studies have shown that ginsenoside Rb1 has neurotrophic and neuroprotective effects. However, whether it influences energy metabolism after spinal cord injury remains unclear. In this study, we treated mouse and cell models of spinal cord injury with ginsenoside Rb1. We found that ginsenoside Rb1 remarkably inhibited neuronal oxidative stress, protected mitochondria, promoted neuronal metabolic reprogramming, increased glycolytic activity and ATP production, and promoted the survival of motor neurons in the anterior horn and the recovery of motor function in the hind limb. Because sirtuin 3 regulates glycolysis and oxidative stress, mouse and cell models of spinal cord injury were treated with the sirtuin 3 inhibitor 3-TYP. When Sirt3 expression was suppressed, we found that the therapeutic effects of ginsenoside Rb1 on spinal cord injury were remarkably inhibited. Therefore, ginsenoside Rb1 is considered a potential drug for the treatment of spinal cord injury, and its therapeutic effects are closely related to sirtuin 3.
| S-EPMC9838172 | biostudies-literature
Project description:ContextObesity, one of the major public health problems worldwide, has attracted increasing attention. Ginsenoside Rb1 is the most abundant active component of Panax ginseng C.A.Mey (Araliaceae) and is reported to have beneficial effects on obesity and diabetes. However, the mechanisms by which Rb1 regulates obesity remain to be explored.ObjectiveThis paper intends to further explore the mechanism of Rb1 in regulating obesity.Materials and methodsThe C57BL/6 obese mice were divided into two groups: the control (CTR) and Rb1. The CTR group [intraperitoneally (ip) administered with saline] and the Rb1 group (ip administered with Rb1, 40 mg/kg/d) were treated daily for four weeks. In vitro, Rb1 (0, 10, 20, 40 μM) was added to differentiated C2C12 cells and Rb1 (0, 20, 40 μM) was added to 3T3-L1 cells. After 24 h, total RNA and protein from C2C12 cells and 3T3-L1 cells were used to detect myostatin (MSTN) and fibronectin type III domain-containing 5 (FNDC5) expression.ResultsRb1 reduced the body weight and adipocyte size. Improved glucose tolerance and increased basic metabolic activity were also found in Rb1 treated mice. MSTN was downregulated in differentiated C2C12 cells, 3T3-L1 cells and adipose tissues upon Rb1 treatment. FNDC5 was increased after Rb1 treatment. However, MSTN overexpression attenuated Rb1-mediated decrease accumulation of lipid droplets in differentiated 3T3-L1 adipocytes.Discussion & conclusionsRb1 may ameliorate obesity in part through the MSTN/FNDC5 signalling pathway. Our results showed that Rb1 can be used as an effective drug in the treatment of human obesity.
| S-EPMC9176416 | biostudies-literature
Project description:Ginsenoside Rb1is the main component in ginsenosides. It is a protopanaxadiol-type ginsenoside that has a dammarane-type triterpenoid as an aglycone. In this study, ginsenoside Rb1 was transformed into gypenoside XVII, ginsenoside Rd, ginsenoside F2 and compound K by glycosidase from Leuconostoc mesenteroides DC102. The optimum time for the conversion was about 72 h at a constant pH of 6.0 to 8.0 and the optimum temperature was about 30℃. Under optimal conditions, ginsenoside Rb1 was decomposed and converted into compound K by 72 h post-reaction (99%). The enzymatic reaction was analyzed by highperformance liquid chromatography, suggesting the transformation pathway: ginsenoside Rb1→ gypenoside XVII and ginsenoside Rd→ginsenoside F2→compound K.
| S-EPMC3659545 | biostudies-literature