ginsenoside-rg2 and Disease-Models--Animal

Alzheimer's disease (AD) is the most common form of dementia, and ginsenoside Rg2 (Rg2) is proven to inhibit AD's progression. This study investigates the potential benefits of Rg2 treatment on 3xTg-AD mice. Following 6 weeks of gavage treatment, Rg2-treated 3xTg-AD mice exhibited improved spatial recognition memory behaviors, regional cerebral blood flow, and histopathological injury of the hippocampus, which were observed through a Y-maze test, laser Doppler flowmetry, and hematoxylin-eosin staining. Additionally, Rg2 treatment caused a decrease in the levels of amyloid beta 25-35, TNF-α, IL-1β, and IL-6, as measured by enzyme-linked immunosorbent assay, as well as a reduction in mRNA levels of IL-1β and IL-6 in 3xTg-AD mouse brains using quantitative real-time PCR. In particular, NeuN and CD31 levels were inhibited and GFAP level was elevated in 3xTg-AD mice that were observed through immunofluorescence, and these levels were all antagonized by Rg2, suggesting the effects of Rg2 on neurovascular damage, astrocyte activation, and neuronal loss. Furthermore, Western blot and qRT-PCR assays showed that Rg2 blocked the expression of ICAM-1 and VCAM-1 in 3xTg-AD mice. By Western blot, the ratios of p-ERK/ERK and p-MAPK/MAPK in 3xTg-AD mice were upregulated by Rg2 treatment, suggesting the neuroprotective effects of Rg2 may be related to the MAPK-ERK pathway. In summary, this study demonstrated the potential of Rg2 to improve AD and provided a scientific basis for research on the biological mechanism of AD and the development of Rg2.

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Disease Models, Animal; Interleukin-6; MAP Kinase Signaling System; Mice; Mice, Transgenic

The present study was performed to investigate the protective effects of ginsenoside Rg2 against Aβ

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Apoptosis; Cognitive Dysfunction; Disease Models, Animal; Ginsenosides; Male; Memory Disorders; Neurons; Neuroprotective Agents; Peptide Fragments; Phosphatidylinositol 3-Kinase; Proto-Oncogene Proteins c-akt; Rats; Rats, Sprague-Dawley; Signal Transduction

The incidence of maternal hemorrhagic stroke is elevated in women with preeclampsia during pregnancy. Panax ginseng is a traditional medicinal herb with numerous applications, and ginsenosides are the key bioactive compounds in Panax ginseng. This study aims to evaluate the effects of ginsenoside Rg2 on pregnancy outcomes and brain injury after intracerebral hemorrhage (ICH) in a rat model of preeclampsia. Preeclampsia was induced in rats by N(ω)-nitro-L-arginine methyl ester. Then, an ICH model was prepared by intrastriatal injection of bacterial collagenase. Ginsenoside Rg2 markedly elevated the survival ratio of fetuses. The placental and body weights were increased in the ginsenoside Rg2 group. Compared with the preeclampsia group, the Garcia test score of ginsenoside Rg2-treated rats was significantly increased. Ginsenoside Rg2 treatment ameliorated the ICH-induced augmentation of Evans blue extravasation, inhibited the ICH-induced elevation of brain water content, and reduced the interleukin-1β and tumor necrosis factor-α levels in the hemorrhagic hemisphere after ICH in preeclampsia model rats. Furthermore, ginsenoside Rg2 treatment not only inhibited augmentation of TLR-4, MyD88, p-IκBα, and p-NF-κB expression but also abated the reduction of occludin and claudin-5 expression in the hemorrhagic hemisphere. The findings indicated that ginsenoside Rg2 improved pregnancy outcomes in a rat model of preeclampsia without decreasing the blood pressure and urine protein level. The findings also demonstrated that ginsenoside Rg2 ameliorated ICH-induced neurological disorder and blood-brain barrier dysfunction in an animal model of preeclampsia by regulating the TLR4/NF-κB signaling pathway.

Topics: Animals; Blood-Brain Barrier; Brain Injuries; Cerebral Hemorrhage; Disease Models, Animal; Female; Ginsenosides; Inflammation Mediators; Pre-Eclampsia; Pregnancy; Rats; Rats, Sprague-Dawley

Post traumatic stress disorder (PTSD) is one of the mental illness. The antidepressant-like properties of ginsenoside Rg2 (GRg2) have been shown, while little is known about its anti-PTSD-like effects. In the present study, the PTSD-associated behavioral deficits in rats were induced following exposure to single prolonged stress (SPS). The results showed that the decreased time and entries in the open arms in elevated plus maze test (EPMT) and increased freezing duration in contextual fear paradigm (CFP) were reversed by GRg2 (10 and 20 mg/kg) without affecting the locomotor activity. In addition, GRg2 (10 and 20 mg/kg) could block the decreased levels of progesterone, allopregnanolone, serotonin (5-HT), 5-Hydroxyindoleacetic acid (5-HIAA), corticotropin releasing hormone (CRH), corticosterone (Cort) and adrenocorticotropic hormone (ACTH) in the brain or serum. In summary, GRg2 alleviated the PTSD-associated behavioral deficits with biosynthesis of neurosteroids, normalization of serotonergic system and HPA axis dysfunction.

Topics: Adrenocorticotropic Hormone; Animals; Anti-Anxiety Agents; Antidepressive Agents; Corticosterone; Corticotropin-Releasing Hormone; Disease Models, Animal; Fear; Ginsenosides; Hydroxyindoleacetic Acid; Locomotion; Male; Maze Learning; Rats; Rats, Sprague-Dawley; Serotonin; Stress Disorders, Post-Traumatic

Major depression is a common neuropsychiatric disease with high lifetime prevalence and high incidence of suicide. This study aimed to evaluate the antidepressant effects of ginsenoside Rg2 in mice, and the possible mechanism was also determined. A single injection of both Rg2 (10 and 20mg/kg) and fluoxetine (positive control, 20mg/kg) induced notable antidepressant-like effects in the forced swim test and tail suspension test without affecting the locomotor activity of mice, and the tests were done 30min after the injection. Also, repeated daily treatment of Rg2 and fluoxetine for the last 2 weeks fully reversed the chronic mild stress (6 weeks)-induced depressive-like symptoms in mice. Moreover, western blot analysis showed that Rg2 administration significantly increased the BDNF signaling pathway in hippocampus. Importantly, the usage of TrkB shRNA fully blocked the antidepressant effects of Rg2 in mice. Collectively, these results suggest that Rg2 produces an antidepressant-like effect in mice which is mediated, at least in part, through promoting the hippocampal BDNF signaling pathway.

Topics: Animals; Antidepressive Agents; Blotting, Western; Brain-Derived Neurotrophic Factor; Chronic Disease; Depressive Disorder; Disease Models, Animal; Dose-Response Relationship, Drug; Fluoxetine; Ginsenosides; Hippocampus; Male; Mice, Inbred C57BL; Stress, Psychological

Ginsenosides, the major active ingredients of Panax ginseng, produce a variety of pharmacological or physiological responses with effects on the central and peripheral nervous systems.. In this report, we investigated the effects of ginsenoside Rg2 on cerebral ischemia-reperfusion induced impairment of neurological responses, memory and caudate-putamen neuronal apoptosis in a vascular dementia (VD) rat model.. Neurological evaluation was performed 24h after reperfusion and Y-maze memory performance was assessed at 48 h after reperfusion. Immunocytochemical techniques were employed to check the protein expression of BCL-2, BAX, heat shock protein 70 and P53, which are related with cell apoptosis.. Neurological responses and memory ability of the ginsenoside Rg2 or nimodipine groups improved significantly compared with the VD group. The expression of BCL-2 and HSP70 were decreased, while BAX and P53 were increased in the VD model. The expression of BCL-2 and HSP70 proteins were increased, while BAX and P53 decreased after ginsenoside Rg2 (2.5, 5 and 10mg/kg) and nimodipine (50 microg/kg) treatment compared with the VD group. The study suggests that ginsenoside Rg2 improved neurological performance and memory ability of VD rats through mechanisms related to anti-apoptosis.. The capacity for ginsenoside Rg2 to modulate the expression of apoptotic related proteins suggests that ginsenoside Rg2 may represent a potential treatment strategy for vascular dementia or other ischemic insults.

Topics: Animals; Apoptosis; bcl-2-Associated X Protein; Dementia, Vascular; Disease Models, Animal; Dose-Response Relationship, Drug; Gene Expression Regulation; Ginsenosides; HSP70 Heat-Shock Proteins; Male; Memory Disorders; Nimodipine; Panax; Proto-Oncogene Proteins c-bcl-2; Random Allocation; Rats; Rats, Sprague-Dawley; Tumor Suppressor Protein p53; Vasodilator Agents