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Vitis Vinifera Leaf Extract Protects Against Glutamate-Induced Oxidative Toxicity in HT22 Hippocampal Neuronal Cells and Increases Stress Resistance Properties in Caenorhabditis Elegans.

ABSTRACT: Vitis vinifea has been used for traditional medicines, food, beverages, and dietary antioxidant supplements. The chemical compositions and biological activities of the fruits and seeds have been extensively investigated. However, the biological effects of the leaves are limited, and its anti-neurodegeneration or antiaging activities are little known. The current work aims to study the beneficial effects of V. vinifera leaf extract on neuroprotective effects in HT22 cells, antiaging, and oxidative stress resistance properties in the Caenorhabditis elegans model. The ethanol extract was characterized by phytochemical composition using gas/liquid chromatography-mass spectrometry and reversed-phase high-performance liquid chromatography. The beneficial effects of V. vinifera ethanol (VVE) extract on antioxidant properties, neuroprotective effects, and the underlying mechanisms were studied by in vitro and in vivo studies. In HT22 cells, we found that VVE has a protective effect against glutamate-mediated oxidative stress-induced cell death. The gene expression of cellular antioxidant enzymes such as CAT, SODs, GSTs, and GPx was upregulated by VVE treatment. Moreover, VVE was also shown to alleviate oxidative stress and attenuate reactive oxygen species accumulation in C. elegans. We demonstrated that VVE could upregulate the expression of stress-response genes gst-4 and sod-3 and downregulate the expression of hsp-16.2. Our results suggest that the oxidative stress resistance properties of VVE are possibly involved in DAF-16/FoxO transcription factors. VVE reduced age-related markers (lipofuscin) while did not extend the life span of C. elegans under normal conditions. This study reports the neuroprotective effect and antioxidant activity of V. vinifera leaf extract and suggests its potential as a dietary or alternative supplement to defend against oxidative stress and age-related diseases.

SUBMITTER: Duangjan C

PROVIDER: S-EPMC8225951 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Grapes and their products are known to have been used for the treatment of diseases throughout history.It was aimed to investigate the effects of Erzincan Cimin grapes on an organism model of Caenorhabditis elegans N2 wild type and C. elegans BS913 strains with gonad cancer.The effects of methanol extracts of the skin and seeds of Erzincan Cimin grapes were examined separately on C. elegans N2 wild type and an effect was determined on lifespan. By applying GS-MS analysis, a potential agent substance was determined in the skin and seed methanol extracts. This substance was purchased and the effects of this substance were investigated on lifespan and fertility in C. elegans BS913 strains with gonad cancer. In addition, the effects on young subjects exposed to this agent substance in L1 form were investigated.Grape seed and skin methanol extract was observed to prolong the lifespan most at a dose of 10 mg/100 mL. Lifespan was determined to be at a maximum in a gonad cancer organism model with benzothiazol at a dose of 50 ppm. At the same dose, positive effects were determined on the fertility of strains with cancer. When the effects of benzothiazol were examined on young L1 forms, an evident retardation of growth was determined at doses of 10, 50, and 100 ppm.Owing to anti-carcinogenic effects of benzothiazol and benzothiazol-derived substances, they can be considered as agent substances in academic studies related to cancer.The effects of methanol extracts of the skin and seeds of Erzincan Cimin grapes were examined on C. elegans N2 wild type and an effect was determined on lifespanThrough GS-MS analysis, benzothiazol was determined in the skin methanol extractsBenzothiazol was purchased and the effects of this substance were investigated on lifespan and fertility in C. elegans BS913 strains with gonad cancerThe effects on young subjects exposed to benzothiazol in L1 formGrape seed, skin methanol extract, and benzothiazol was observed to prolong the lifespanPositive effects were determined on the fertility of gonad cancer strains. Abbreviations used: GC-MS: gas chromatography and mass spectrometry; C. elegans: Caenorhabditis elegans; NGM: Nematode growth medium; E. coli: Escherichia coli; FUDR: Fluorodeoxyuridine; LDL: Low-density lipoprotein.

Project description:In traditional herbal medicine, the Polyscias fruticosa has been frequently used for the treatment of ischemia and inflammation. Oxidative stress mediated by elevated glutamate levels cause neuronal cell death in ischemia and various neurodegenerative diseases. However, so far, the neuroprotective effects of this plant extract against glutamate-mediated cell death have not been investigated in cell models. The current study investigates the neuroprotective effects of ethanol extracts of Polyscias fruticosa (EEPF) and elucidates the underlying molecular mechanisms of EEPFs relevant to neuroprotection against glutamate-mediated cell death. The oxidative stress-mediated cell death was induced by 5 mM glutamate treatment in HT22 cells. The cell viability was measured by a tetrazolium-based EZ-Cytox reagent and Calcein-AM fluorescent dye. Intracellular Ca2+ and ROS levels were measured by fluorescent dyes, fluo-3 AM and 2',7'-dichlorodihydrofluorescein diacetate (DCF-DA), respectively. Protein expressions of p-AKT, BDNF, p-CREB, Bax, Bcl-2, and apoptosis-inducing factor (AIF) were determined by western blot analysis. The apoptotic cell death was measured by flow cytometry. The in vivo efficacy of EEPF was evaluated using the Mongolian gerbil mouse by surgery-induced brain ischemia. EEPF treatment showed a neuroprotective effect against glutamate-induced cell death. The EEPF co-treatment reduced the intracellular Ca2+ and ROS and apoptotic cell death. Furthermore, it recovered the p-AKT, p-CREB, BDNF, and Bcl-2 levels decreased by glutamate. The EEPF co-treatment suppressed the activation of apoptotic Bax, the nuclear translocation of AIF, and mitogen-activated protein kinase (MAPK) pathway proteins (ERK1/2, p38, JNK). Further, EEPF treatment significantly rescued the degenerative neurons in the ischemia-induced Mongolian gerbil in vivo model. EEPF exhibited neuroprotective properties that suppress glutamate-mediated neurotoxicity. The underlying mechanism of EEPF is increasing the level of p-AKT, p-CREB, BDNF, and Bcl-2 associated with cell survival. It has therapeutic potential for the treatment of glutamate-mediated neuropathology.

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Vitis Vinifera Leaf Extract Protects Against Glutamate-Induced Oxidative Toxicity in HT22 Hippocampal Neuronal Cells and Increases Stress Resistance Properties in Caenorhabditis Elegans.

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