• Journal of the Society of Cosmetic Scientists of Korea
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• v.48 no.4
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• pp.373-383
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• 2022

Inflammation caused by active oxygen and the resulting barrier damage have been consistently pointed out as the cause of wrinkle formation. In this study, effective index ingredient search and efficacy analysis were performed to verify the value of use as a functional cosmetic material related to antioxidant, anti-inflammatory and skin barrier improvement, and anti-aging for extracts of four types of Eleutherococcus divaricatus var. chiisanensis (ED), Eleutherococcus senticosus (EN), Eleutherococcus sessiliflorus (ES), and Eleutherococcus sieboldianus (EI) belonging to the Eleutherococcus genus. To identify the effective index composition, the content of the ingredients was measured by high-performance liquid chromatography. The content of eleutheroside E and chlorogenic acid was the highest in ED among the Eleutherococcus genus. As for anti-oxidant activity, DPPH radical scavenging activity was the highest in ED. In anti-inflammatory effects, ED extracts inhibited nitric oxide generation in inflammatory macrophage cells due to lipopolysaccharide by 40% at 100 ㎍/mL. In the case of IL-6 inhibition, which is known as a pro-inflammatory cytokine, ED showed 41% inhibition at 100 ㎍/mL. In addition, filaggrin and involucrin, which are skin barrier-related factors, were increased by 2.5 times and 1.6 times, respectively, in 100 ㎍/mL of ED extracts, and as for the collagenase, which is a wrinkle-related factor, ED extract showed 29% efficacy at 100 ㎍/mL. Thus, these result suggested that ED extract, among the four Eleutherococcus genus, can be used as a cosmetic ingredient for suppressing inflammation in the skin, reinforcing the skin barrier, and reducing wrinkles.

• 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.

• Tuberculosis and Respiratory Diseases
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• v.42 no.5
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• pp.646-653
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• 1995

Background: The confirmative diagnosis of pulmonary tuberculosis(Tb) can be made by the isolation of Mycobacterium Tuberculosis(MTb) in the culture of the sputum, respiratory secretions or tissues of the patients, but positive result could not always be obtained in pulmonary Tb cases. Although there are many indirect ways of the diagnosis of Tb, clinicians still experience the difficulty in the diagnosis of Tb because each method has its own limitation. Therefore development of a new diagnostic tool is clinically urgent. It was reported that silica cause some lysosomal enzymes to be released from macrophages in vitro and one of these enzymes is elevated in workers exposed to silica dust and in silicotic subjects. In pulmonary Tb, alveolar macrophages are known to be activated after ingestion of MTb. Activated macrophages can kill MTb through oxygen free radical species and digestive enzymes of lysosome. But if macrophages allow the bacilli to grow intracellularly, the macrophages will die finally and local lesion will enlarge. Then it is assumed that the lysosomal enzymes would be released from the dead macrophages. The goal of this investigation was to determine if there are differences in the plasma activities of lysosomal enzymes, ($\beta$-glucuronidase(GLU) and $\beta$-N-acetyl glucosaminidase(NAG), among the groups of active and inactive pulmonary Tb and healthy control, and to see if there is any possibility that the plasma activity of GLU and NAG can be used as diagnostic indicies of active pulmonary Tb. Methods: The plasma were obtained from 20 patients with bacteriologically proven active pulmonary Tb, 15 persons with inactive Tb and 20 normal controls. In 10 patients with active pulmonary Tb, serial samples after 2 months of anti-Tb medications were obtained. Plasma GLU and NAG activities were measured by the fluorometric methods using 4-methylumbelliferyl substrates. All data are expressed as the mean $\pm$ the standard error of the mean. Results: The activites of GLU and NAG in plasma of the patients with active Tb were $21.52{\pm}3.01$ and $325.4{\pm}23.37$(nmol product/h/ml of plasma), respectively. Those of inactive pulmonary Tb were $24.87{\pm}3.78$, $362.36{\pm}33.92$ and those of healthy control were $25.45{\pm}4.05$, $324.44{\pm}28.66$(nmol product/h/ml of plasma), respectively. There were no significant differences in the plasma activities of both enzymes among 3 groups. The plasma activities of GLU at 2 months after anti-Tb medications were increased($42.18{\pm}5.94$ nmol product/h/ml of plasma) in the patients with active pulmonary Tb compared with that at the diagnosis of Tb(P-value <0.05). Conclusion: The results of the present investigation suggest that the measurement of the plasma activities of GLU and NAG in the patients with active pulmonary Tb could not be a useful method for the diagnosis of active Tb. Further investigation is necessary to define the reasons why the plasma activities of the GLU was increased in the patients with active pulmonary Tb after Tb therapy.

• 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.