• Title/Summary/Keyword: Cytoxicity

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The Study on the Potential Anti-aging Properties of Prunella vulgaris Extract In Vitro and In Vivo (하고초 추출물의 항노화 효과에 관한 연구)

  • Hong, Eun-Suk;Ahn, Gi-Woong;Jo, Byoung-Kee
    • Journal of the Society of Cosmetic Scientists of Korea
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    • v.34 no.2
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    • pp.129-135
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    • 2008
  • In this study, the potential anti-aging properties of Prunella vulgaris extract were investigated. According to our results, Prunella vulgaris extract increased collagen synthesis(74.7% at 250 ${\mu}g/mL$) and decreased on MMP-1 synthesis(90.2% at 200 ${\mu}g/mL$) and elastase activity(43.7% at 2.0%). Furthermore, it also showed free radical scavenging activity(76.9% at 2.0%) and reduced $H_2O_2$-induced cytoxicity(49.9% at 2.0%). A double-blind clinical study to investigate the effect of Prunella vulgaris extract on the skin's surface was conducted with 22 healthy volunteers, aged 34 to 48 years. The volunteers applied a cream formula with 4.0% of Prunella vulgaris extract, or placebo cream, on each crow's feet twice a day for 12 weeks. Skin wrinkles were evaluated with the naked eye and instrumental image analysis of silicone replicas, followed by statistical analysis. Twelve weeks after application of cream formula with 4.0% of Prunella vulgaris extract, we found significant improvement of facial wrinkle. Moreover, silicone replica analysis confirmed notable improvement in average of R2 and R3 at 12 weeks(p<0.05). These results demonstrate that Prunella vulgaris provides a remarkable and significant tensor and anti-wrinkle effect on the skin, which could be of great use in anti-aging skin care products.

Cellular protective effect of Ecklonia cava extract on ultra-fine dust (PM2.5)-induced cytoxicity (초미세먼지(PM2.5)로 유도된 in vitro 세포 독성에 대한 감태(Ecklonia cava) 추출물의 보호 효과)

  • Park, Seon Kyeong;Kang, Jin Yong;Kim, Jong Min;Yoo, Seul Ki;Han, Hye Ju;Shin, Eun Jin;Heo, Ho Jin
    • Korean Journal of Food Science and Technology
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    • v.51 no.5
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    • pp.503-508
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    • 2019
  • To evaluate the protective effect of Ecklonia cava on ultra-fine dust ($PM_{2.5}$)-induced cytotoxicity, we investigated the in vitro antioxidant activity and cell viability after exposure to $PM_{2.5}$. E. cava was extracted using water and 80% ethanol, and antioxidant activity was determined using the 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid) (ABTS)/2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging and lipid peroxidation inhibition assays. The 80% ethanol extract showed relatively higher antioxidant activity than the water extract. The cell protective effects were determined by measuring the intracellular reactive oxygen species (ROS) content and viability of nasal epithelial (RPMI-2650), lung epithelial (A549), and brain neuroblastoma (MC-IXC) cells. Results showed that the 80% ethanol extract inhibited ROS production more than the water extract. In contrast, both extracts showed similar effects on cell viability in the $PM_{2.5}$-induced cell death assay. Thus, Ecklonia cava may act as an effective resource for preventing $PM_{2.5}$-induced cytotoxicity in nasal, lung, and brain cells.

Protective effects of Aruncus dioicus var. kamtschaticus extract against hyperglycemic-induced neurotoxicity (포도당 처리로 유도된 뇌신경세포 독성에 대한 눈개승마 추출물의 보호효과)

  • Park, Su Bin;Lee, Uk;Kang, Jin Yong;Kim, Jong Min;Park, Seon Kyeong;Park, Sang Hyun;Choi, Sung-Gil;Heo, Ho Jin
    • Korean Journal of Food Science and Technology
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    • v.49 no.6
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    • pp.668-675
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    • 2017
  • To assess the physiological effects of Aruncus dioicus var. kamtschaticus extract on cytoxicity of a neuronal cell line, antioxidant activity, and neuroprotection against intensive glucose-induced oxidative stress were quantitated. Compared to the other fractions, the ethyl acetate fraction of Aruncus dioicus var. kamtschaticus (EFAD) showed the highest total phenolics and flavonoids. The 2,2-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) assay and malondialdehyde inhibitory effect test confirmed the superior antioxidant activity of EFAD. Moreover, EFAD also decreased the intracellular ROS level and suppressed neuronal cell death against intensive glucose- or $H_2O_2$-induced oxidative stress. Additionally, assessment of ${\alpha}$-glucosidase and acetylcholinesterase inhibitory activities revealed that EFAD was an effective inhibitor of ${\alpha}$-glucosidase and acetylcholinesterase. Finally, high-performance liquid chromatography analysis identified caffeic acid as the main ingredient of EFAD. Overall, these results suggest that the EFAD is a good natural source of biological compounds that counteract hyperglycemic neuronal defects.

Characterization of Nitric Oxide (NO)-Induced Cell Death in Lung Epithelial Cells (폐상피세포에서 Nitric Oxide (NO)에 의한 세포사에 관한 연구)

  • Yong, Wha Shim;Kim, Youn Seup;Park, Jae Seuk;Jee, Young Koo;Lee, Kye Young
    • Tuberculosis and Respiratory Diseases
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    • v.56 no.2
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    • pp.187-197
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    • 2004
  • Background : Nitric Oxide (NO) is a multi-faceted molecule with dichotomous regulatory roles in many areas of biology. NO can promote apoptosis in some cells, whereas it inhibits apoptosis in other cell types. This study was performed to characterize NO-induced cell death in lung epithelial cells and to investigate the roles of cell death regulators including iron, bcl-2 and p53. Methods : A549 cells were used for lung epithelial cells. SNP (sodium nitroprusside) and SNAP (S-nitroso-N-acetyl- penicillamine) were used for NO donor. Cytoxicity assay was done by MTT assay and crystal violet assay. Apoptotic assay was done by fluorescent microscopy after double staining with propidium iodide and hoecst 33342. Iron inhibition study was done with RBCs and FeSO4. For bcl-2 study, bcl-2 overexpressing cells (A549-bcl-2) were used and for p53 study, Western blot analysis and p53 functionally knock-out cells (A549-E6) were used. Results : SNP and SNAP induced dose-dependent cell death in A549 cells and fluorescent microscopy revealed that SNAP induced apoptosis in low doses but necrosis in high doses while SNP induced exclusively necrotic cell death. Iron inhibition study using RBCs and FeSO4 significantly blocked SNAP-induced cell death. And also SNAP-induced cell death was blocked by bcl-2 overexpression. Finally, we found that SNAP activate p53 by Western blot analysis and that SNAP-induced cell death was decreased in the abscence of p53. Conclusion : In lung epithelial cells, NO can induce cell death, more precisely apoptosis in low doses and necrosis in high doses. And iron, bcl-2, and p53 play important roles in NO-induced cell death.