• Journal of Microbiology and Biotechnology
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• 제27권7호
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• pp.1257-1265
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• 2017

The present study was carried out to investigate the antioxidative and neuroprotective effects of sea buckthorn (Hippophae rhamnoides L.) leaves (SBL) harvested at different times. Reversed-phase high-performance liquid chromatography analysis revealed five major phenolic compounds: ellagic acid, gallic acid, isorhamnetin, kaempferol, and quercetin. SBL harvested in August had the highest total phenolic and flavonoid contents and antioxidant capacity. Treatment of neuronal PC-12 cells with the ethyl acetate fraction of SBL harvested in August increased their viability and membrane integrity and reduced intracellular oxidative stress in a dose-dependent manner. The relative populations of both early and late apoptotic PC-12 cells were decreased by treatment with the SBL ethyl acetate fraction, based on flow cytometry analysis using annexin V-FITC/PI staining. These findings suggest that SBL can serve as a good source of antioxidants and medicinal agents that attenuate oxidative stress.

• 생약학회지
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• 제53권2호
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• pp.79-86
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• 2022

Excessive glutamate causes oxidative stress in neuronal cells, which can cause degenerative neurological disorders. We tried to find medicinal plant showed neuroprotective activity by using glutamate-injured HT22 cell as a model system. In this study, we found that Boesenbergia rotunda methanol extract showed neuroprotective activity against glutamate induced neurotoxicity in mouse hippocampal HT22 cells. B. rotunda methanol extract suppressed the formation of reactive oxygen species and decreased intracellular Ca²⁺concentration. Also, B. rotunda made mitochondrial membrane potential maintain to normal levels. In addition, B. rotunda increased total glutathione amount and activated antioxidative enzyme such as glutathione reductase and glutathione peroxidase compared to glutamate-treated groups. These results suggested that B. rotunda decreased neuronal cell death damaged by high concentrations of glutamate treatment, via antioxidative mechanism and might be one of candidate of development of new drug to treat neurodegenerative disease such as Alzheimer's disease.

• Biomolecules & Therapeutics
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• 제19권4호
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• pp.451-459
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• 2011

Peroxiredoxins (Prxs) have a critical role in protecting cells against oxidative damage generated by reactive oxygen species (ROS). PrxI and PrxII are more than 90% homologous in their amino acid sequences, and both proteins reduce $H_2O_2$. In this study, an over-expression plasmid carrying PrxI was transfected into $PrxII^{-/-}$ mouse embryonic fibroblasts (MEFs) to investigate potential compensatory relationships between PrxI and PrxII. ROS levels induced by oxidative stress were increased in $PrxII^{-/-}$ MEFs as compared to wild-type MEFs. Moreover, exposure of $PrxII^{-/-}$ MEFs to $H_2O_2$ caused a reduction in cell viability of about 10%, and the proportion of cell death was increased compared to mock-treated $PrxII^{-/-}$ MEFs. However, transient over-expression of PrxI in $PrxII^{-/-}$ MEFs conferred increased resistance against the oxidative damage, as evidenced by increased cell viability and reduced intracellular ROS levels under $H_2O_2$ stress conditions. The findings suggest that over-expressed PrxI can partly compensate for the loss of PrxII function in PrxII-deficient MEFs.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 2003년도 Annual Meeting of KSAP : International Symposium on Pharmaceutical and Biomedical Sciences on Obesity
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• pp.65-65
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• 2003

The aim of this study was to investigate the effect of resveratrol on the oxidative stress-induced inhibition of gap junctional intercellular communication (GJIC) in HaCaT keratinocyte. Anti-oxidative activity of resveratrol was measured by a,a-diphenyl-b-picrylhydrazyl (DPPH) assay and dichlorodihydrofluorescein diacetate oxidation assay. GJIC of HaCaT keratinocyte was assessed using the scrape loading/dye transfer technique. Western blots and reverse transcription-polymerase chain reaction were also analyzed for Connexin 43 protein and mRNA expression, respectively. Resveratrol scavenged directly the stable DPPH radical over a concentration range of 4 mg/$\mell$ (78.2 $\pm$ 2.7% of control) to 500 mg/$\mell$ (29.9 $\pm$ 4.2% of control) and prevent to increase the intracellular fluorescence induced by oxidative stress significantly. Ultraviolet A irradiation (UVA) and 12-O-tetradecanoylphorbol-13-acetate markedly reduced GJIC, which was restored by resveratrol. There were no significant differences in the level of Connexin 43 protein and mRNA expression among any of the experimental groups. Our data suggests that resveratrol has the protective effect on the oxidative stress-induced inhibition of gap junctional intercellular communication in HaCaT keratinocyte and this protection is likely due to the scavenging of reactive oxygen species.

• Nutrition Research and Practice
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• 제14권1호
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• pp.3-11
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• 2020

BACKGROUND/OBJECTIVES: Oxidative stress causes cell damage and death, which contribute to the pathogenesis of neurodegenerative diseases. Urolithin A (UA), a gut microbial-derived metabolite of ellagitannins and ellagic acid, has high bioavailability and various health benefits such as antioxidant and anti-inflammatory effects. However, it is unknown whether it has protective effects against oxidative stress-induced cell death. We investigated whether UA ameliorates H₂O₂-induced neuronal cell death. MATERIALS/METHODS: We induced oxidative damage with 300 μM H₂O₂ after UA pretreatment at concentrations of 1.25, 2.5, and 5 μM in SK-N-MC cells. Cytotoxicity and cell viability were determined using the CCK-8 assay. The formation of reactive oxygen species (ROS) was measured using a 2,7-dichlorofluorescein diacetate assay. Hoechst 33342 staining was used to characterize morphological changes in apoptotic cells. The expressions of apoptosis proteins were measured using Western blotting. RESULTS: UA significantly increased cell viability and decreased intracellular ROS production in a dose-dependent manner in SK-N-MC cells. It also decreased the Bax/Bcl-2 ratio and the expressions of cytochrome c, cleaved caspase-9, cleaved caspase-3, and cleaved PARP. In addition, it suppressed the phosphorylation of the p38 mitogen-activated protein kinase (MAPK) pathway. CONCLUSIONS: UA attenuates oxidative stress-induced apoptosis via inhibiting the mitochondrial-related apoptosis pathway and modulating the p38 MAPK pathway, suggesting that it may be an effective neuroprotective agent.

• Biomolecules & Therapeutics
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• 제11권4호
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• pp.224-231
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• 2003

The aim of this study was to investigate the effect of resveratrol on the oxidative stress-induced inhibition of gap junctional intercellular communication in HaCaT keratinocytes. Anti-oxidative activity of resveratrol was measured by $\alpha,\alpha$-diphenyl-$\beta$-picrylhydrazyl assay and dichlorodihydrofluorescein diacetate oxidation assay. Gap junctional intercellular communication in HaCaT keratinocytes was assessed using the scrape loading/dye transfer technique. Western blots and reverse transcription-polymerase chain reaction were also analyzed for connexin 43 protein and mRNA expression, respectively. Resveratrol scavenged directly the stable $\alpha,\alpha$-diphenyl-$\beta$-picrylhydrazyl radical over a concentration range of 4 mg/ml ($78.2{\pm}2.7$% of control) to 500 mg/ml ($29.9{\pm}4.2$% of control) and decreased the intracellular reactive oxygen species induced by ultraviolet A (UVA) irradiation ($89.3{\pm}1.1$% of UVA group), ultraviolet B (UVB) irradiation ($70.9{\pm}1.7$% of UVB group) and 12-0-tet-radecanoylphorbol-13-acetate (TPA, $48.3{\pm}1.1$% of TPA group), respectively. UVA irradiation and TPA markedly reduced gap junctional intercellular communication, which was restored by resveratrol. There were no significant differences in the level of connexin 43 protein and mRNA expression among any of the experimental groups. Our data suggests that resveratrol has the protective effect on the oxidative stress-induced inhibition of gap junctional intercellular communication in HaCaT keratinocytes, and this protection is likely due to the scavenging of reactive oxygen species.

• 한국축산식품학회지
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• 제44권3호
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• pp.699-709
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• 2024

Oxya chinensis sinuosa (OC) is a well-known edible insect. Several researches on the health benefits of OC consumption have been performed to date; however, their effect on eye health remains largely unknown. This study aimed to assess the protective effects of OC extracts on the oxidative stress on the retinal pigment epithelium (RPE) cells. Oxidative damage has been identified as one of the key regulatory factors in agerelated macular degeneration. H₂O₂-induced reactive oxygen species (ROS) production, a well-known oxidative stress factor, can cause cell death in retinal pigment epithelia cells. In this study, we found that three OC extracts effectively prevented H₂O₂-induced ROS production and subsequent death of ARPE-19 cells in a dose-dependent manner. In addition, the OC extracts inhibited the phosphorylation of mitogen-activated protein kinases including p38, JNK, and ERK. The OC extracts restored IκBα degradation induced by H₂O₂, indicating that OC extracts suppressed the activation of nuclear factorκB. Furthermore, the three OC extracts were shown to have antioxidant effects by upregulating the intracellular expression of key antioxidant proteins such as SOD, NQO, and HO-1. Here we demonstrated the antioxidant and anti-apoptotic effects of the OC extracts on ARPE-19, indicating their potential role in improving eye health. These results suggest that three OC extracts plays a critical role in oxidative stress-induced cell death protects in ARPE-19 cells.

• Asian Pacific Journal of Cancer Prevention
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• 제16권8호
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• pp.3213-3222
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• 2015

Background: Cancer metastasis depends on cell motility which is driven by cycles of actin polymerization and depolymerization. Reactive oxygen species (ROS) and metabolic oxidative stress have long been associated with cancer. ROS play a vital role in regulating actin dynamics that are sensitive to oxidative modification. The current work aimed at studying the effects of sub-lethal metabolic oxidative stress on actin cytoskeleton, focal adhesion and cell migration. Materials and Methods: T47D human breast cancer cells were treated with 2-deoxy-D-glucose (2DG), L-buthionine sulfoximine (BSO), or doxorubicin (DOX), individually or in combination, and changes in intracellular total glutathione and malondialdehyde (MDA) levels were measured. The expression of three major antioxidant enzymes was studied by immunoblotting, and cells were stained with fluorescent-phalloidin to evaluate changes in F-actin organization. In addition, cell adhesion and degradation ability were measured. Cell migration was studied using wound healing and transwell migration assays. Results: Our results show that treating T47D human breast cancer cells with drug combinations (2DG/BSO, 2DG/DOX, or BSO/DOX) decreased intracellular total glutathione and increased oxidized glutathione, lipid peroxidation, and cytotoxicity. In addition, the drug combinations caused a reduction in cell area and mitotic index, prophase arrest and a decreased ability to form invadopodia. The formation of F-actin aggregates was increased in treated T47D cells. Moreover, combination therapy reduced cell adhesion and the rate of cell migration. Conclusions: Our results suggest that exposure of T47D breast cancer cells to combination therapy reduces cell migration via effects on metabolic oxidative stress.

• Environmental Analysis Health and Toxicology
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• 제22권1호
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• pp.57-64
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• 2007

Nanomaterials have been used to create unique devices at the nanoscale level. However, the toxicities of nanomaterials have not been fully tested and the risk of nanomaterials has been raised as an emerging issue in these days. In this study, the cytotoxicity of silver nanoparticles was tested using cultured mouse leydig cells. As results, silver nanoparticles showed cytotoxicity with the generation of reactive oxygen species (ROS). With the increased level of ROS, intracellular glutathione level was decreased. DNA fragmentation and caspase-3 activation suggested the apoptotic mechanism of cell death in leydig cells treated with silver nanoparticles.

• 한국해양생명과학회지
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• 제7권2호
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• pp.113-120
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• 2022

Despite concerns about the significant toxicity of copper pyrithione (CuPT) at environmental concentrations, effects of CuPT on benthic organisms have received little attention. Here, we analyzed the detrimental effects of CuPT at sublethal concentrations (1/50, 1/20, and 1/10 of the 96 h-LC50 value) for 14 days in the marine polychaete Perinereis aibuhitensis. Reduced burrowing activity and significantly decreased the acetylcholinesterase activity in response to relatively high concentrations of CuPT were identified as CuPT-triggered cholinergic inhibition. The lipid peroxidation marker, malondialdehyde levels were dose-dependently increased, whereas intracellular glutathione was depleted by relatively high concentrations. In the CuPT-treated polychaete, significant fluctuations in the enzymatic activities of the antioxidant defense system (catalase, superoxide dismutase, glutathione reductase, and glutathione peroxidase) were observed with significantly modulated glutathione 𝘚-transferase activity. These results indicate that even sublethal levels of CuPT would have detrimental effects on the health status of the marine polychaete.