Ginsenoside Rb2 suppresses the glutamate-mediated oxidative stress and neuronal cell death in HT22 cells

Kim, Dong Hoi; Kim, Dae Won; Jung, B.; Lee, Jong-Hun; Lee, Heesu; Hwang, Gwi Seo; Kang, Ki Sung; Lee, Jae Woo

doi:10.1016/j.jgr.2018.12.002

Cited by 64 publications

(48 citation statements)

References 45 publications

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“…The amount of the formazan dye, generated by the activities of dehydrogenases in cells, is directly proportional to the number of living cells. Cell viability was determined through the change of absorbance measured at 450 nm using PowerWave XS microplate reader (Bio-Tek Instruments, Winooski, VT, USA) [27].…”

Section: Cell Viability Assaymentioning

confidence: 99%

Effect of Herbal Formulation on Immune Response Enhancement in RAW 264.7 Macrophages

Trinh

Park

et al. 2020

Biomolecules

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Immune response is a necessary self-defense mechanism that protects the host from infectious organisms. Many medicinal plants are popularly used in Asian folk medicine to increase body resistance. An herbal formulation named KM1608 was prepared from three medicinal plants: Saussurea lappa, Terminalia chebula, and Zingiber officinale. In this study, we evaluated the immune stimulatory effect of KM1608 on RAW 264.7 murine macrophages. Network pharmacological analyses were used to predict potential immune response pathways of major compounds from KM1608. The cytotoxicity and immuno-stimulating effect of KM1608 were determined using cell viability and nitric oxide assays. The underlying mechanism of immunomodulatory activity was evaluated by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) of pro-inflammatory cytokines. The results of network pharmacological analysis suggested that major compounds from KM1608 possess anticancer potential via immune signaling pathways. After treatment with KM1608 at 25–100 µg/mL for 24 h, the level of nitric oxide was increased in the dose-dependent manner. The results of quantitative real-time PCR showed that KM1608 stimulates the expression of immune cytokines (interferon (IFN)-α, -β, IL-1β, -6, IL-10, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2)) in macrophages. KM1608 extract is a potential agent for immune response enhancement.

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Section: Cell Viability Assaymentioning

confidence: 99%

Effect of Herbal Formulation on Immune Response Enhancement in RAW 264.7 Macrophages

Trinh

Park

et al. 2020

Biomolecules

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“…Sample-induced nuclear condensation of HCT-116 cells was observed using Hoechst 33342 staining (Sigma Aldrich, St. Louis, MO, USA) [20]. Briefly, the cells were seeded in a 6-well plate at 4 × 10 5 cells per well.…”

Section: Hoechst 33342 Cell Stainingmentioning

confidence: 99%

Analysis and Identification of Active Compounds from Salviae miltiorrhizae Radix Toxic to HCT-116 Human Colon Cancer Cells

et al. 2020

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Colorectal cancer is one of the most frequently diagnosed cancers worldwide. The aim of the present study was to simultaneously analyze compounds of Salviae miltiorrhizae Radix (SMR) and determine their cytotoxic effects on HCT-116 human colorectal cancer cells. We established a simultaneous analysis method of five compounds (salvianic acid A, salvianolic acid B, caffeic acid, tanshinone IIA, and rosmarinic acid) contained in SMR, and found that among the various compounds in SMR, tanshinone IIA significantly decreased cell viability in a concentration-dependent manner. Hoechst staining also showed that both SMR and tanshinone IIA increased nuclear condensation, suggesting induction of apoptosis. By Western blotting, we found that tanshinone IIA induced apoptotic cell death, significantly increased Bax, but decreased Bcl-2 in the course of apoptosis. Tanshinone IIA increased the expression of cleaved caspases-7 and -8. Tanshinone IIA was shown to be an active ingredient of SMR that may be a useful chemotherapeutic strategy for patients with colorectal cancer.

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“…A murine hippocampal cell line, HT22 cells, were grown in Dulbecco's modified Eagle's medium (DMEM; Corning, Manassas, VA, USA) supplemented with 10% fetal bovine serum (Atlas, Fort Collins, CO, USA) and antibiotics (streptomycin/penicillin; Gibco, Grand Island, NY, USA). HT22 cells were maintained at 37 • C in a humidified incubator supplied with 5% CO 2 [29]. The experimental conditions containing incubation times were determined according to the results of measuring each marker at various time points [15].…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

Neuroprotective Effects of Tetrahydrocurcumin against Glutamate-Induced Oxidative Stress in Hippocampal HT22 Cells

et al. 2019

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In the central nervous system, glutamate is a major excitable neurotransmitter responsible for many cellular functions. However, excessive levels of glutamate induce neuronal cell death via oxidative stress during acute brain injuries as well as chronic neurodegenerative diseases. The present study was conducted to examine the effect of tetrahydrocurcumin (THC), a major secondary metabolite of curcumin, and its possible mechanism against glutamate-induced cell death. We prepared THC using curcumin isolated from Curcuma longa (turmeric) and demonstrated the protective effect of THC against glutamate-induced oxidative stress in HT22 cells. THC abrogated glutamate-induced HT22 cell death and showed a strong antioxidant effect. THC also significantly reduced intracellular calcium ion increased by glutamate. Additionally, THC significantly reduced the accumulation of intracellular oxidative stress induced by glutamate. Furthermore, THC significantly diminished apoptotic cell death indicated by annexin V-positive in HT22 cells. Western blot analysis indicated that the phosphorylation of mitogen-activated protein kinases including c-Jun N-terminal kinase, extracellular signal-related kinases 1/2, and p38 by glutamate was significantly diminished by treatment with THC. In conclusion, THC is a potent neuroprotectant against glutamate-induced neuronal cell death by inhibiting the accumulation of oxidative stress and phosphorylation of mitogen-activated protein kinases.Molecules 2020, 25, 144 2 of 10 neurodegenerative diseases [3,4]. Earlier studies showed that an excessive release of glutamate in the extracellular region provoked the accumulation of intracellular ROS by depletion of intracellular glutathione levels through blocking cysteine uptake [5]. The presence of an antioxidant, such as flavonoids or N-acetylcysteine, strongly prevented ROS-induced neuronal cell death [6,7].The use of natural antioxidants for scavenging free radicals and maintaining homeostasis contributes to alleviating neuronal dysfunction [8]. Typically, natural compounds are multiple-target molecules found mainly in microorganisms and plants and exhibit strong antioxidant activity [8,9]. Phenolic compounds from natural sources also exhibit various beneficial effects in cancer, inflammation, and neurodegenerative disorders [9]. This broad spectrum of biological or pharmacological activities has made phytochemicals suitable candidates for treating multifactorial diseases, such as neurodegenerative diseases [10,11]. However, there are also several concerns regarding their poor bioavailability, stability and safety, which must be resolved before effective therapeutics can be developed.Mitogen-activated protein kinases (MAPKs), known as a family of serine/threonine protein kinases, are well-identified biological molecules involved in glutamate-induced oxidative neuronal cell death. MAPKs are related to multiple cellular functions including differentiation, proliferation, cell survival, inflammation, and cell death [12]. The presence of excessive glutam...

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Ginsenoside Rb2 suppresses the glutamate-mediated oxidative stress and neuronal cell death in HT22 cells

Cited by 64 publications

References 45 publications

Effect of Herbal Formulation on Immune Response Enhancement in RAW 264.7 Macrophages

Effect of Herbal Formulation on Immune Response Enhancement in RAW 264.7 Macrophages

Analysis and Identification of Active Compounds from Salviae miltiorrhizae Radix Toxic to HCT-116 Human Colon Cancer Cells

Neuroprotective Effects of Tetrahydrocurcumin against Glutamate-Induced Oxidative Stress in Hippocampal HT22 Cells

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