• 동의생리병리학회지
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• 제25권2호
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• pp.280-293
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• 2011

There is currently increased interest in the identification of antioxidant compounds that are pharmacologically potent and have low or no side effects. Plants produce significant amounts of antioxidants to prevent the oxidative stress caused by photons and oxygen, therefore they represent a potential source of new compounds with antioxidant activity. FARFARE FLOS has been frequently used on the respiratory system including bronchitis, phthisis. In this study, the antioxidant activity of extract from FF was studied in vitro methods by measuring the antioxidant activity by TEAC, measuring the scavenging effects on reactive oxygen species (ROS) [superoxide anion, hydroxyl radical] and on reactive nitrogen species (RNS) [nitric oxide and peroxynitrite] as well as measuring the inhibitory effect on Cu2+-induced human LDL oxidation. The FF extracts were found to have a potent scavenging activity, as well as an inhibitory effect on LDL oxidation. And this study was designed to evaluate whether FFEA may ameliorate oxidative stress and inflammatory status through the antioxidative mechanism in LPS-stimulated RAW 264.7 murine macrophage cell line. Treatment of RAW 264.7 cells with FFEA significantly reduced LPS-stimulated inflammatory response in a dose-dependent manner. In conclusion, the FF extracts have anti-oxidative and anti-inflammatory effects in vitro system, which can be used for developing pharmaceutical drug against oxidative stress and atherosclerosis.

• 치위생과학회지
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• 제19권3호
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• pp.198-204
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• 2019

Background: Oxidative stress is a known to be associated with in the pathogenesis of many inflammatory diseases, including periodontitis. Ursolic acid is a pentacyclic triterpenoid with has antimicrobial, antioxidative, and anticancer properties. However, the role of ursolic acid in the regulating of osteogenesis remains undetermined. This study was aimed to elucidate the crucial osteogenic effects of ursolic acid and its ability to inhibit oxidative stress by targeting the immediate early response 3 (IER3)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Methods: Cell proliferation was determined using water-soluble tetrazolium salt assay, cell differentiation was evaluated by alkaline phosphatase (ALP) activity, and formation of calcium nodules was detected using alizarin red S stain. Generation of reactive oxygen species (ROS) was determined using by DCFH-DA fluorescence dye in hydrogen peroxide ($H_2O_2$)-treated MG-63 cells. Expression levels of IER3, Nrf2, and heme oxygenase-1 (HO-1) were analyzed using western blot analysis. Results: Our results showed that ursolic acid up-regulated the proliferation of osteoblasts without any cytotoxic effects, and promoted ALP activity and mineralization. $H_2O_2$-induced ROS generation was found to be significantly inhibited on treatment with ursolic acid. Furthermore, in $H_2O_2$-treated cells, the expression of the early response genes: IER3, Nrf2, and Nrf2-related phase II enzyme (HO-1) was enhanced in the presence of ursolic acid. Conclusion: The key findings of the present study elucidate the protective effects of ursolic acid against oxidative stress conditions in osteoblasts via the IER3/Nrf2 pathway. Thus, ursolic acid may be developed as a preventative and therapeutic agent for mineral homeostasis and inflammatory diseases caused due to oxidative injury.

• Journal of Yeungnam Medical Science
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• 제40권2호
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• pp.115-122
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• 2023

Hepatic ischemia-reperfusion injury is a major complication of liver transplantation, trauma, and shock. This pathological condition can lead to graft dysfunction and rejection in the field of liver transplantation and clinical hepatic dysfunction with increased mortality. Although the pathological mechanisms of hepatic ischemia-reperfusion injury are very complex, and several intermediators and cells are involved in this phenomenon, oxidative stress and inflammatory responses are the key processes that aggravate hepatic injury. This review summarizes the current understanding of oxidative stress and inflammatory responses and, in that respect, addresses the therapeutic approaches to attenuate hepatic ischemia-reperfusion injury.

• Journal of Periodontal and Implant Science
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• 제50권5호
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• pp.291-302
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• 2020

Purpose: The objective of this study was to investigate whether phelligridin D could reduce glucose-induced oxidative stress, attenuate the resulting inflammatory response, and restore the function of human periodontal ligament cells (HPDLCs). Methods: Primary HPDLCs were isolated from healthy human teeth and cultured. To investigate the effect of phelligridin D on glucose-induced oxidative stress, HPDLCs were treated with phelligridin D, various concentrations of glucose, and glucose oxidase. Glucose-induced oxidative stress, inflammatory molecules, osteoblast differentiation, and mineralization of the HPDLCs were measured by hydrogen peroxide (H₂O₂) generation, cellular viability, alkaline phosphatase (ALP) activity, alizarin red staining, and western blot analyses. Results: Glucose-induced oxidative stress led to increased production of H₂O₂, with negative impacts on cellular viability, ALP activity, and calcium deposition in HPDLCs. Furthermore, HPDLCs under glucose-induced oxidative stress showed induction of inflammatory molecules (intercellular adhesion molecule-1, vascular cell adhesion protein-1, tumor necrosis factor-alpha, interleukin-1-beta) and disturbances of osteogenic differentiation (bone morphogenetic protein-2, and -7, runt-related transcription factor-2), cementogenesis (cementum protein-1), and autophagy-related molecules (autophagy related 5, light chain 3 I/II, beclin-1). Phelligridin D restored all these molecules and maintained the function of HPDLCs even under glucose-induced oxidative stress. Conclusions: This study suggests that phelligridin D reduces the inflammation that results from glucose-induced oxidative stress and restores the function of HPDLCs (e.g., osteoblast differentiation) by upregulating autophagy.

• Animal Bioscience
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• 제34권2호
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• pp.312-319
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• 2021

Objective: Stress-induced cytotoxicity caused by xenobiotics and endogenous metabolites induces the production of reactive oxygen species and often results in damage to cellular components such as DNA, proteins, and lipids. The cytochrome P450 (CYP) family of enzymes are most abundant in hepatocytes, where they play key roles in regulating cellular stress responses. We aimed to determine the effects of the antioxidant compound, methylsulfonylmethane (MSM), on oxidative stress response, and study the cytochrome P450 family 3 subfamily A (CYP3A) gene expression in fetal horse hepatocytes. Methods: The expression of hepatocyte markers and CYP3A family genes (CYP3A89, CYP3A93, CYP3A94, CYP3A95, CYP3A96, and CYP3A97) were assessed in different organ tissues of the horse and fetal horse liver-derived cells (FHLCs) using quantitative reverse transcription polymerase chain reaction. To elucidate the antioxidant effects of MSM on FHLCs, cell viability, levels of oxidative markers, and gene expression of CYP3A were investigated in H2O2-induced oxidative stress in the presence and absence of MSM. Results: FHLCs exhibited features of liver cells and simultaneously maintained the typical genetic characteristics of normal liver tissue; however, the expression profiles of some liver markers and CYP3A genes, except that of CYP3A93, were different. The expression of CYP3A93 specifically increased after the addition of H2O2 to the culture medium. MSM treatment reduced oxidative stress as well as the expression of CYP3A93 and heme oxygenase 1, an oxidative marker in FHLCs. Conclusion: MSM could reduce oxidative stress and hepatotoxicity in FHLCs by altering CYP3A93 expression and related signaling pathways.

• Molecules and Cells
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• 제45권7호
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• pp.454-464
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• 2022

DJ-1 is one of the causative genes of early-onset familial Parkinson's disease (PD). As a result, DJ-1 influences the pathogenesis of sporadic PD. DJ-1 has various physiological functions that converge to control the levels of intracellular reactive oxygen species (ROS). Based on genetic analyses that sought to investigate novel antioxidant DJ-1 downstream genes, pyruvate dehydrogenase (PDH) kinase (PDK) was demonstrated to increase survival rates and decrease dopaminergic (DA) neuron loss in DJ-1 mutant flies under oxidative stress. PDK phosphorylates and inhibits the PDH complex (PDC), subsequently downregulating glucose metabolism in the mitochondria, which is a major source of intracellular ROS. A loss-of-function mutation in PDK was not found to have a significant effect on fly development and reproduction, but severely ameliorated oxidative stress resistance. Thus, PDK plays a critical role in the protection against oxidative stress. Loss of PDH phosphatase (PDP), which dephosphorylates and activates PDH, was also shown to protect DJ-1 mutants from oxidative stress, ultimately supporting our findings. Further genetic analyses suggested that DJ-1 controls PDK expression through hypoxia-inducible factor 1 (HIF-1), a transcriptional regulator of the adaptive response to hypoxia and oxidative stress. Furthermore, CPI-613, an inhibitor of PDH, protected DJ-1 null flies from oxidative stress, suggesting that the genetic and pharmacological inhibition of PDH may be a novel treatment strategy for PD associated with DJ-1 dysfunction.

• Journal of Plant Biotechnology
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• 제50권
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• pp.76-81
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• 2023

As cultured plant cells can grow in high oxidative stress conditions, they form an excellent system to study antioxidant mechanisms and the mass production of antioxidants. Oxidative stress is a major cause of damage in plants exposed to various types of environmental stress, including heavy metals, such as cadmium (Cd). Heavy metal accumulation can interfere with many cell functions and plant growth. To evaluate the contribution of oxidative stress to Cd-induced toxicity, cultured sweetpotato (Ipomoea batatas) cells were treated with increasing concentrations of Cd (0, 10, 25, and 50 μM) and cultured further. Cell growth was significantly inhibited by 25 and 50 μM of Cd, and the total protein content increased with 50 μM of Cd. Additionally, the activity of peroxidase (POD) and ascorbate peroxidase (APX), antioxidant enzymes that remove hydrogen peroxide (a reactive oxygen species), increased in the cells after treatment with 50 μM of Cd. The expression analysis of POD, APX, and peroxiredoxin (PRX) isolated from sweetpotato cultured cells in a previous study revealed the differential expression of POD in response to Cd. In this study, the expression levels of several acidic POD (swpa2, swpa3, and swpa4) and basal POD (swpb1, swpb2, and swpb3) genes were increased in Cd-treated cultured cells. These results indicate that Cd-mediated oxidative stress is closely linked to improved POD-mediated antioxidant defense capacity in sweetpotato suspension-cultured cells.

• 한국초지조사료학회지
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• 제42권3호
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• pp.208-214
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• 2022

Drought stress is a condition that occurs frequently in the field, it reduces of the agricultural yield of field crops. The aim of the study was to screen drought-adapted genotype of Italian rye grass. The experiments were conducted between the two Italian ryegrass (Lolium multiflorum L.) cultivars viz. Hwasan (H) and Kowinearly (KE). The plants were exposed to drought for 14 days. The results suggest that the morphological traits and biomass yield of KE significantly affected by drought stress-induced oxidative stress as the hydrogen peroxide (H₂O₂) level was induced, while these parameters were unchanged or less affected in H. Furthermore, the cultivar H showed better adaptation by maintaining several physiological parameter including photosystem-II (Fv/Fm), water use efficiency (WUE) and relative water content (RWC%) level in response to drought stress. These results indicate that the cultivar H shows improved drought tolerance by generic variation, improving photosynthetic efficiency and reducing oxidative stress damages under drought stress. These findings can be useful to the breeder and farmer for improving drought tolerance in Italian rye grass through breeding programs.

• Biomolecules & Therapeutics
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• 제17권4호
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• pp.395-402
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• 2009

Insulin appears to play a role in brain physiology, and disturbances of cerebral insulin signalling and glucose homeostasis are implicated in brain pathology. The objective of the present study was to investigate the protective effects of insulin under conditions of oxidative stress induced by hydrogen peroxide ($H_2O_2$) in C6 glial cells. Insulin at concentration of $10^{-7}$ M could prevent 12 h $H_2O_2$-induced cell death. The formation of reactive oxygen species (ROS), nitric oxide (NO) and 2-thiobarbituric acid-reactive substances (TBARS) were significantly scavenged by insulin pre-treatment in C6 glial cells after $H_2O_2$-induced oxidative stress. Insulin significantly stimulated the phosphorylation of Akt in the cells and the activation of Akt was maintained in response to insulin under $H_2O_2$ incubation for 12 h. In conclusion, these results provide evidence that insulin acts as a free radical scavenger and stimulating Akt activity. These data suggest that insulin may be effective in degenerative diseases with oxidative stress.

• Biomolecules & Therapeutics
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• 제9권4호
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• pp.249-257
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• 2001

The effect of oxidative stress on the alterations of different antioxidant enzyme activities was investigated in human skin melanoma cell line (SK-MEL-2). Oxidative stress was induced by the exposure to hydrogen peroxide ($H_2O$$_2$). SK-MEL-2 cells were treated with antioxidants such as vitamin E and selenomethionine in combination with $H_2O$$_2$. SK-MEL-$_2$ cells were exposed to various concentrations of $H_2O$$_2$ and measured the time course of changes in cell viability and antioxidant enzyme activities for 24 hr. Oxidative stress was induced by the exposure to 2.5mM hydrogen peroxide ($H_2O$$_2$) resulted in declining significantly for 24 hr. GPX and CAT activities peaked at 3 hr and returned to control levels by 24 hr. On the contrary, SOD activity was inactive before 6 hr but recovered at 24 hr. In case vitamin E (Vit E) and selenomethionine (Se-Met) were used at nontoxic concentrations (25$\mu$M Vit E/500$\mu$M Se-Met) to oxidative stress was induced by the exposure to hydrogen peroxide ($H_2O$$_2$) led to a 3- and 5-fold increase on the viability comparing to control and caused an increase in GPX activity respectively.