• Journal of Life Science
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• v.32 no.4
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• pp.310-317
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• 2022

Recently, interest in the harmful factors of particulate matter (PM), a major component of air pollution, has been increasing. In particular, PM_2.5 with a diameter of less than 2.5 ㎛ is well known to induce oxidative stress accompanied by autophagy in human lung epithelial cells. However, studies on whether PM_2.5 increases autophagy under oxidative stress and whether this process is reactive oxygen species (ROS)-dependent are insufficient. Therefore, in this study, we investigated whether PM_2.5 promotes autophagy through the generation of ROS in human alveolar epithelial A594 cells. According to our results, cells co-treated with PM_2.5 and hydrogen peroxide (H₂O₂) showed a lower cell viability than cells treated with each alone, which was associated with increased total and mitochondrial ROS production. The co-treatment of PM_2.5 and H₂O₂ also increased autophagy induction, which was confirmed through Cyto-ID staining, and the expression of autophagy biomarker proteins increased. However, when ROS generation was artificially blocked by N-acetyl-L-cysteine pretreatment, the reduction in cell viability and induction of autophagy by PM_2.5 and H₂O₂ co-treatment were markedly attenuated. Therefore, the present results suggest that PM_2.5-induced ROS generation may play a critical role in autophagy induction in A549 cells.

• Food Science and Preservation
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• v.31 no.1
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• pp.183-196
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• 2024

This study investigated the protective effect of the aqueous extract of Eucommia ulmoides leaves (AEEL) against high glucose-induced human colon epithelial HT-29 cells. The 2,2'-azino-bis (3-ethyl benzothiazoline-6-sulfonic acid) (ABTS), 1,1-diphenyl-2-picrylhydrazy (DPPH) radical scavenging activities, ferric reducing/antioxidant power (FRAP), and malondialdehyde (MDA) analyses indicated that AEEL had significant antioxidant activities. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showed that AEEL increased cell viability against high glucose-, H₂O₂-, and lipopolysaccharide (LPS)-induced cytotoxicity in HT-29 cells. Also, the 2'-7'-dichlorodihydrofluorescein diacetate (DCF-DA) assay indicated that AEEL decreased intracellular reactive oxygen species (ROS) against high glucose-, H₂O₂-, and lipopolysaccharide (LPS)-induced cytotoxicity in HT-29 cells. AEEL showed inhibitory activities against α-glucosidase and inhibited the formation of advanced glycation end products (AGEs). AEEL showed significant positive effects on the viability and titratable acidity of L. brevis. The high-performance liquid chromatogram (HPLC) analysis identified chlorogenic acid and rutin as the major compounds of AEEL. These results suggested that AEEL has the potential to be used as a functional food source to suppress blood glucose levels and protect the gut from high glucose-induced oxidative stress.

• Korean Journal of Plant Resources
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• v.37 no.2
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• pp.120-129
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• 2024

Alcoholic liver disease (ALD) is a significant risk factor in the global disease burden. The stem bark of the Betulaceae plant Alnus japonica, which is indigenous to Korea, has been used as a popular folk medicine for hepatitis and cancer. However, the preventive effect of Alnus japonica leaf extracts on alcohol-related liver damage has not been investigated. The objective of this study was to investigate the hepatoprotective effects of the extracts of Alnus japonica leaf (AJL) against ethanol-induced liver damage in HepG2/2E1 cells. Treatment with AJL significantly prevented ethanol-induced cytotoxicity in HepG2/2E1 cells by reducing the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). This protective effect was likely associated with antioxidant potential of AJL, as evidenced by the attenuation of reactive oxygen species (ROS) and malondialdehyde (MDA) production and restoration of the depleted glutathione (GSH) levels in ethanol-induced HepG2/2E1 cells. Our findings suggest that FCC might be considered as a useful agent in the prevention of liver damage induced by oxidative stress by increasing the antioxidant defense mechanism.

• Journal of Food Hygiene and Safety
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• v.26 no.3
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• pp.260-265
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• 2011

Plantago asiatica L. (P. asiatica) has been used as one of the popular folk medicines in Asia for human health care practices. Various activities of P. asiatica have been reported, such as anti-oxidant, anti-glycation, anti-inflammatory and hepatoprotective activity. Therefore, the potential of P. asiatica to reduce oxidative stress has been studied in several ways for over 20 years, especially at liver and kidney. However no investigation has been reported revealing its protective effect on prostate. Method: Treatment of P. asiatica leaf ethanolic extract (PLE) (1 g/kg body weight (b.w.), 2 g/kg b.w., or 4 g/kg b.w.) were given separately to animals for pretreatment once per day for 7 days, and on the seventh day ferric nitrilotriacetate (Fe-NTA; 0.24 mmol Fe/kg b.w.), which is known as an oxidative stress-inducer at prostate, was administrated by i.p to negative control group. At the end of the study period, dissection was carried out for detecting the prostate protective effect of PLE. Result: Fe-NTA-treated animals produced reactive oxygen species (ROS) resulting in depletion of antioxidant biomaker, such as glutathione (GSH), glutathione reductase (GR), and glutathione s-transferase (GST) and increase of lipid peroxidation in prostate. However, PLE pretreatment resulted in an increase in the GSH, GST and GR levels concentration dependent manner and in an significant decrease in the levels of lipid peroxidation. Conclusion: Our data suggest that PLE may be effective in protecting oxidative stress-induced damage of prostate, and PLE may be an chemopreventive agent against Fe-NTA-mediated prostate oxidative damage.

• Tuberculosis and Respiratory Diseases
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• v.60 no.4
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• pp.451-463
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• 2006

Background : Reactive oxygen species (ROS) take center stage as executers in ventilator-induced lung injury (VILI). The protein with DNA-damage scanning activity, poly (ADP-ribose) polymerase-1 (PARP1), signals DNA rupture and participates in base-excision repair. Paradoxically,overactivation of PARP1 in response to massive genotoxic injury such as ROS can induce cell death through ${\beta}$ -nicotinamide adenine dinucleotide ($NAD^+$) depletion, resulting in inflammation. The purpose of this study is to investigate the role of PARP1 and the effect of its inhibitor in VILI. Methods : Forty-eight male C57BL/6 mice were divided into sham, lung protective ventilation(LPV), VILI, and PARP1 inhibitor (PJ34)+VILI (PJ34+VILI) groups. Mechanical ventilator setting for the LPV group was $PIP\;15cmH_2O$ + $PEEP\;3cmH_2O$ + RR 90/min + 2 hours. The VILI and PJ34+VILI groups were ventilated on a setting of $PIP\;40cmH_2O$ + $PEEP\;0cmH_2O$ + RR 90/min + 2 hours. As a PARP1 inhibitor for the PJ34+VILI group, 20 mg/Kg of PJ34 was treated intraperitoneally 2 hours before mechanical ventilation. Wet-to-dry weight ratio and acute lung injury (ALI) score were measured to determine the degree of VILI. PARP1 activity was evaluated by using an immunohistochemical method utilizing biotinylated NAD. Myeloperoxidase (MPO) activity and the concentration of inflammatory cytokines such as tumor necrosis factor $(TNF)-{\alpha}$, interleukin $(IL)-1{\beta}$, and IL-6 were measured in bronchoalveolar lavage fluid (BALF). Results : In the PJ34+VILI group, PJ34 pretreatment significantly reduced the degree of lung injury, compared with the VILI group (p<0.05). The number of cells expressing PARP1 activity was significantly increased in the VILI group, but significantly decreased in the PJ34+VILI group (p=0.001). In BALF, MPO activity, $TNF-{\alpha}$, $IL-1{\beta}$, and IL-6 were also significantly lower in the PJ34+VILI group (all, p<0.05). Conclusion : PARP1 overactivation plays a major role in the mechanism of VILI. PARP1 inhibitor prevents VILI, and decreases MPO activity and inflammatory cytokines.

• Korean Journal of Soil Science and Fertilizer
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• v.16 no.1
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• pp.20-27
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• 1983

A series of laboratory experiment was conducted to find out the chemical composition, characterization of humic substances by physical and chemical methods and reaction of Na-pyrophosphate, $Ca(OH)_2$ and rice straw with albumin on the degradation of soil organic matter in the volcanic ask soils of the Jeju Island. Results obtained were summarized as follows: 1. The contents of organic matter, available silicon, active iron and aluminum concentration in volcanic ash the soils were remarkably higher but available phosphorous was comparatively lower than the mineral soils. In volcanic ash soil, the contents of potassium, calcium and magnessium were higher in upland soil than that of forest soil. The ratios of active $Al^{{+}{+}{+}}/Fe^{{+}{+}}$, C/P and $K/Ca^+$ Mg were apparently high in volcanic ash soils while that of $SiO_2$/O.M. was high in mineral soil. 2. The carbon/nitrogen ratio in humin, humic acid content in organic matter, and carbon contents of humin in total carbon of soil organic matter were apparently higher in the volcanic ash soils than in the mineral soils, The total nitrogen and fractions of acid or alkali soluble nitrogen were remarkably high in volcanic ash soils while mineralizable nitrogen ($NH_4$-N and $NO_3$) contents were high in mineral soils. 3. The values of K600, RF and log K were also higher in volcanic ash soils than those in mineral soils, and the absorbance in the visible range were high and color was dark in the soil of which humification was progressed Extracted humic acid from volcanic ash soil was less reactive to the oxidizing chemical reagent and was persistance to the acid or alkali hydrolysises. 4. The major oxygen-containing functional groups in humic substances of volcanic ash soils were phenolic-OH alcoholic-OH and carboxyl groups while those in mineral soil were methoxyl and carbonyl groups. 5. Absorption spectra of alkaline solution of humic acid ranged from 200 nm to maxima 500 nm. Visible spectra peaks of from humic substances in the visible region were recognized at 350, 420, 450 and 480 nm. Only one single absorbance peak was observed in the visible region at 362 nm for Heugag series and two absorbance Peak were also at 360 nm and 390 nm for Yeungrag series. 6. Evolution of carbon as $Co_2$ was increased with addition of Na-pyrophosphate in Namweon and Heugag series, and "priming effects" took place on the soil organic matter decomposition by addition of rice straw with albumin in Ido series.

• Journal of Chest Surgery
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• v.39 no.12 s.269
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• pp.879-890
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• 2006

Background: The dysfunction of multiple organs is found to be caused by reactive oxygen species as a major modulator of microvascular injury after hemorrhagic shock. Hemorrhagic shock, one of many causes inducing acute lung injury, is associated with increase in alveolocapillary permeability and characterized by edema, neutrophil infiltration, and hemorrhage in the interstitial and alveolar space. Aggressive and rapid fluid resuscitation potentially might increased the risk of pulmonary dysfunction by the interstitial edema. Therefore, in order to improve the pulmonary dysfunction induced by hemorrhagic shock, the present study was attempted to investigate how to reduce the inflammatory responses and edema in lung. Material and Method: Male Sprague-Dawley rats, weight 300 to 350 gm were anesthetized with ketamine(7 mg/kg) intramuscular Hemorrhagic Shock(HS) was induced by withdrawal of 3 mL/100 g over 10 min. through right jugular vein. Mean arterial pressure was then maintained at $35{\sim}40$ mmHg by further blood withdrawal. At 60 min. after HS, the shed blood and Ringer's solution or 5% albumin was infused to restore mean carotid arterial pressure over 80 mmHg. Rats were divided into three groups according to rectal temperature level($37^{\circ}C$[normothermia] vs $33^{\circ}C$[mild hypothermia]) and resuscitation fluid(lactate Ringer's solution vs 5% albumin solution). Group I consisted of rats with the normothermia and lactate Ringer's solution infusion. Group II consisted of rats with the systemic hypothermia and lactate Ringer's solution infusion. Group III consisted of rats with the systemic hypothermia and 5% albumin solution infusion. Hemodynamic parameters(heart rate, mean carotid arterial pressure), metabolism, and pulmonary tissue damage were observed for 4 hours. Result: In all experimental groups including 6 rats in group I, totally 26 rats were alive in 3rd stage. However, bleeding volume of group I in first stage was $3.2{\pm}0.5$ mL/100 g less than those of group II($3.9{\pm}0.8$ mL/100 g) and group III($4.1{\pm}0.7$ mL/100 g). Fluid volume infused in 2nd stage was $28.6{\pm}6.0$ mL(group I), $20.6{\pm}4.0$ mL(group II) and $14.7{\pm}2.7$ mL(group III), retrospectively in which there was statistically a significance between all groups(p<0.05). Plasma potassium level was markedly elevated in comparison with other groups(II and III), whereas glucose level was obviously reduced in 2nd stage of group I. Level of interleukine-8 in group I was obviously higher than that of group II or III(p<0.05). They were $1.834{\pm}437$ pg/mL(group I), $1,006{\pm}532$ pg/mL(group II), and $764{\pm}302$ pg/mL(group III), retrospectively. In histologic score, the score of group III($1.6{\pm}0.6$) was significantly lower than that of group I($2.8{\pm}1.2$)(p<0.05). Conclusion: In pressure-controlled hemorrhagic shock model, it is suggested that hypothermia might inhibit the direct damage of ischemic tissue through reduction of basic metabolic rate in shock state compared to normothermia. It seems that hypothermia should be benefit to recovery pulmonary function by reducing replaced fluid volume, inhibiting anti-inflammatory agent(IL-8) and leukocyte infiltration in state of ischemia-reperfusion injury. However, if is considered that other changes in pulmonary damage and inflammatory responses might induce by not only kinds of fluid solutions but also hypothermia, and that the detailed evaluation should be study.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1265-1276
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• 1998

Background : Nitric oxide(NO) is an endogenously produced free radical that plays an important role in regulating vascular tone, inhibition of platelet aggregation and white blood cell adhesion to endothelial cells, and host defense against infection. The highly reactive nature of NO with oxygen radicals suggests that it may either promote or reduce oxidant-induced cell injury in several biological pathways. Oxidant injury and interactions between pulmonary vascular endothelium and leukocytes are important in the pathogenesis of acute lung injury, including acute respiratory distress syndrome(ARDS). In ARDS, therapeutic administration of NO is a clinical condition providing exogenous NO in oxidant-induced endothelial injury. The role of exogenous NO from NO donor or the suppression of endogenous NO production was evaluated in oxidant-induced endothelial injury. Method : The oxidant injury in cultured rat lung microvascular endothelial cells(RLMVC) was induced by hydrogen peroxide generated from glucose oxidase(GO). Cell injury was evaluated by $^{51}$chromium($^{51}Cr$) release technique. NO donor, such as S-nitroso-N-acetylpenicillamine(SNAP) or sodium nitroprusside(SNP), was added to the endothelial cells as a source of exogenous NO. Endogenous production of NO was suppressed with N-monomethyl-L-arginine(L-NMMA) which is an NO synthase inhibitor. L-NMMA was also used in increased endogenous NO production induced by combined stimulation with interferon-$\gamma$(INF-$\gamma$), tumor necrosis factor-$\alpha$(TNF-$\alpha$), and lipopolysaccharide(LPS). NO generation from NO donor or from the endothelial cells was evaluated by measuring nitrite concentration. Result : $^{51}Cr$ release was $8.7{\pm}0.5%$ in GO 5 mU/ml, $14.4{\pm}2.9%$ in GO 10 mU/ml, $32.3{\pm}2.9%$ in GO 15 mU/ml, $55.5{\pm}0.3%$ in GO 20 mU/ml and $67.8{\pm}0.9%$ in GO 30 mU/ml ; it was significantly increased in GO 15 mU/ml or higher concentrations when compared with $9.6{\pm}0.7%$ in control(p < 0.05; n=6). L-NMMA(0.5 mM) did not affect the $^{51}Cr$ release by GO. Nitrite concentration was increased to $3.9{\pm}0.3\;{\mu}M$ in culture media of RLMVC treated with INF-$\gamma$ (500 U/ml), TNF-$\alpha$(150 U/ml) and LPS($1\;{\mu}g/ml$) for 24 hours ; it was significantly suppressed by the addition of L-NMMA. The presence of L-NMMA did not affect $^{51}Cr$ release induced by GO in RLMVC pretreated with INF-$\gamma$, TNF-$\alpha$ and LPS. The increase of $^{51}Cr$ release with GO(20 mU/ml) was prevented completely by adding 100 ${\mu}M$ SNAP. But the add of SNP, potassium ferrocyanate or potassium ferricyanate did not protect the oxidant injury. Nitrite accumulation was $23{\pm}1.0\;{\mu}M$ from 100 ${\mu}M$ SNAP at 4 hours in phenol red free Hanks' balanced salt solution. But nitrite was not detectable from SNP upto 1 mM The presence of SNAP did not affect the time dependent generation of hydrogen peroxide by GO in phenol red free Hanks' balanced salt solution. Conclusion : Hydrogen peroxide generated by GO causes oxidant injury in RLMVC. Exogenous NO from NO donor prevents oxidant injury, and the protective effect may be related to the ability to release NO. These results suggest that the exogenous NO may be protective on oxidant injury to the endothelium.