• 제목/요약/키워드: Premature aging

검색결과 49건 처리시간 0.027초

A Rapid and Sensitive Screening System for Human Type I Collagen with the Aim of Discovering Potent Anti-Aging or Anti-Fibrotic Compounds

  • Hashem, Md. Abul;Jun, Kyu-Yeon;Lee, Eunyoung;Lim, Soyun;Park Choo, Hea-Young;Kwon, Youngjoo
    • Molecules and Cells
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    • 제26권6호
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    • pp.625-630
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    • 2008
  • This study was undertaken with the aim of developing an easy and quick means of analyzing the effect of various compounds on the synthesis and secretion of human type I collagen at the protein level. A modification of the ELISA method was used on HFF-1 cells. For the proof of concept, we used thirteen compounds most of which are known to be antioxidants. Each compound was tested at concentrations of 0, 10 and $100{\mu}m$ on HFF-1 cells for 24 h. Thirteen sets of experiments for each compound were performed in ANOVA with three replicates. Duncan multiple range test (DMRT) was used to compare the mean values obtained from the treatment groups. From the results it was concluded that Vitamin C, undecylenic acid, conjugated linoleic acid, glycolic acid, and citric acid at $100{\mu}m$ concentration could be used for anti-wrinkling or protection from premature aging, which requires enhancement of collagen synthesis. Lactic acid, EGCG, resveratrol, and retinol that can inhibit collagen synthesis effectively in a dose-dependent manner may be used for anti-fibrosis treatment purposes.

Anti-Wrinkling Effect of Noni (Morinda citrifolia) by Antioxidant and Anti-Inflammatory Properties

  • Choi, Soo-Cheol;Youn, Young Han
    • 인간식물환경학회지
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    • 제23권2호
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    • pp.191-199
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    • 2020
  • Noni has been used for medicinal purposes for more than 2,000 years in South Pacific Polynesia, China and India, and has been heavily ingested as an extract for its excellent antioxidant and anti-inflammatory effects. However, a recent study found that the noni extract causes digestive disorders, kidney problems, and liver diseases, which made it necessary to use it for other purposes than as an extract. In this study, we want to evaluate the potential of noni as an anti-oxidant, anti-inflammatory and anti-wrinkling agent. Methods: Noni was freeze-dried, extracted in water, and concentrated. Skin cells were treated with the noni extract for 24 hrs and then were exposed to UVB (55 mJ/cm2). After 48 hrs of incubation, pro-inflammatory cytokine, elastase, MMP-1 and type-1 procollagen levels were measured by ELISA. Results: To find out the antioxidant effect of the noni extract, the DPPH and ABTS radical scavenging activity experiments were conducted and the noni extract showed 97.0 % and 92.0 % antioxidant efficacy at 200 ㎍/mL respectively. The noni extract (50 and 100 ㎍/mL) decreased IL-6 and TNF-α in RAW 264.7 cells induced by LPS in a concentration-dependent manner. In the RT-PCR experiment involving NO production, the noni extract (50 and 100 ㎍/mL) inhibited NO production by strongly inhibiting iNOS mRNA expression, and also inhibited the elevation of MMP-1 and elastases caused by UVB irradiation by 25.0 % and 7.0 % respectively. In addition, type-1 procollagen was elevated by 20.0 % by the noni extract treatment in HaCaT cells. Conclusion: The noni extract has photoprotective ability by reducing proinflammatory mediators, elastase and MMP-1 production, and elevation of collagen synthesis. Our findings suggest that the noni extract might be a good natural substance to protect against UVB-induced premature skin aging.

Hutchison-Gilford 조로증 증후군 환아에서의 뇌 자기공명 혈관조영술 소견: 증례 보고 (Detection of Cerebrovascular Disease in a Child with Hutchinson-Gilford Progeria Syndrome Using MR Angiography: A Case Report)

  • 이재호;이하영;임명관;강영혜
    • 대한영상의학회지
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    • 제83권6호
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    • pp.1360-1365
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    • 2022
  • Hutchinson-Gilford progeria 증후군(syndrome) (이하 HGPS)은 심혈관 및 뇌혈관 질환의 조기 이환율을 갖는 드문 진행성 조기 노화 증후군이다. 임상증상은 매우 다양하여 성장 부진, 경피증, 탈모증, 골다공증과 같은 비특이적 증상 외에도 가속화된 혈관 노화에 의해 유년기 및 청소년기에 발생하는 고혈압과 심뇌혈관 질환을 포함한다. HGPS 환자에게 자기공명 혈관조영술은 무증상 뇌졸중 또는 혈관 변화를 조기에 진단하고 뇌혈관 질환의 위험성 증가를 평가하기 위해 권장된다. 이 증례 보고는 전형적인 임상 특징을 보인 5세 환아에서 유전자분석으로 확진된 국내 두 번째 HGPS이며, 뇌 자기공명 혈관조영술 소견을 제시한 국내 최초 영문 증례 보고이다.

인간피부 섬유아세포에서 UVB 유도된 산화 스트레스와 기질금속단백질가수분해효소 발현에 블루베리의 저해능 (Inhibitory Activity of Blueberries on UVB-induced Oxidative Stress and Matrix Metalloproteinase Expression in Human Skin Fibroblasts)

  • 장영아;김세기
    • 생명과학회지
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    • 제29권12호
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    • pp.1321-1328
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    • 2019
  • 자외선B(UVB: 290-320 nm) 방사선으로도 알려진 중간 파장 태양광선은 인간에게 조기 노화 및 산화손상에 의존하는 피부암을 유발할 수 있다. UVB가 유발하는 반응성 산소종(ROS)의 형성은 종종 이러한 광선에 과도하게 노출되는 결과로 MMP-1과 MMP-3와 같은 매트릭스 금속단백질(MMP)을 활성화할 수 있다. 이 효소들은 인간의 섬유질에서 type 1형 콜라겐을 분해한다. 본 연구에서는 블루베리(EEB)의 에틸 아세테이트 추출물의 항산화 및 항노화 효과를 평가했다. 블루베리의 항산화 실험은 DPPH 분석과 CCD-986sk 세포를 사용하여 ROS 생성을 평가했다. 블루베리의 주름방지 효능을 평가하기 위해 MMP-1 생성과 type 1형 procollagen 합성을 평가하고 Western Blot과 RT- PCR을 통해 MMP 1, 3의 발현량을 평가하였다. EEB는 2,2-diphenyl-1-picrylhydrazyl (DPPH) 라디칼의 소거능을 보이며 UVB에 유도된 ROS의 생성을 저해하였다. 또한 EEB는 procollagen 생성감소 및 MMP-1 생성량의 증가 등 광노화 및 피부암과 관련된 UVB로 야기되는 과정을 억제하였다. 더 정확히 말하면, EEB (50㎍/ml)는 MMP-1과 -3의 mRNA와 단백질 발현을 현저히 억제하였다. EEB의 항노화 효과는 항산화 작용에 기인한다. 이러한 연구 결과는 EEB가 type 1형 procollagen, MMP-1, MMP-3의 수준을 조절함으로써 인간 섬유아세포에서 UVB가 유발하는 노화로부터 보호 효과를 가지고 있음을 나타낸다.

Duck Oil-loaded Nanoemulsion Inhibits Senescence of Angiotensin II-treated Vascular Smooth Muscle Cells by Upregulating SIRT1

  • Kang, Eun Sil;Kim, Hyo Juong;Han, Sung Gu;Seo, Han Geuk
    • 한국축산식품학회지
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    • 제40권1호
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    • pp.106-117
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    • 2020
  • Cellular senescence is associated with age-related vascular disorders and has been implicated in vascular dysfunctions. Here, we show that duck oil-loaded nanoemulsion (DO-NE) attenuates premature senescence of vascular smooth muscle cells (VSMCs) triggered by angiotensin II (Ang II). Compared with control nanoemulsion (NE), DO-NE significantly inhibited the activity of senescence-associated β-galactosidase, which is a biomarker of cellular senescence, in Ang II-treated VSMCs. SIRT1 protein expression was dose- and time-dependently induced in VSMCs exposed to DO-NE, but not in those exposed to NE, and SIRT1 promoter activity was also elevated. Consistently, DO-NE also dose-dependently rescued Ang II-induced repression of SIRT1 expression, indicating that SIRT1 is linked to the anti-senescence action of DO-NE in VSMCs treated with Ang II. Furthermore, the SIRT1 agonist resveratrol potentiated the effects of DO-NE on VSMCs exposed to Ang II, whereas the SIRT1 inhibitor sirtinol elicited the opposite effect. These findings indicate that DO-NE inhibits senescence by upregulating SIRT1 and thereby impedes vascular aging triggered by Ang II.

Phloroglucinol Attenuates Free Radical-induced Oxidative Stress

  • So, Mi Jung;Cho, Eun Ju
    • Preventive Nutrition and Food Science
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    • 제19권3호
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    • pp.129-135
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    • 2014
  • The protective role of phloroglucinol against oxidative stress and stress-induced premature senescence (SIPS) was investigated in vitro and in cell culture. Phloroglucinol had strong and concentration-dependent radical scavenging effects against nitric oxide (NO), superoxide anions ($O_2{^-}$), and hydroxyl radicals. In this study, free radical generators were used to induce oxidative stress in LLC-PK1 renal epithelial cells. Treatment with phloroglucinol attenuated the oxidative stress induced by peroxyl radicals, NO, $O_2{^-}$, and peroxynitrite. Phloroglucinol also increased cell viability and decreased lipid peroxidation in a concentration-dependent manner. WI-38 human diploid fibroblast cells were used to investigate the protective effect of phloroglucinol against hydrogen peroxide ($H_2O_2$)-induced SIPS. Phloroglucinol treatment attenuated $H_2O_2$-induced SIPS by increasing cell viability and inhibited lipid peroxidation, suggesting that treatment with phloroglucinol should delay the aging process. The present study supports the promising role of phloroglucinol as an antioxidative agent against free radical-induced oxidative stress and SIPS.

Transcriptional Profiling and Dynamical Regulation Analysis Identify Potential Kernel Target Genes of SCYL1-BP1 in HEK293T Cells

  • Wang, Yang;Chen, Xiaomei;Chen, Xiaojing;Chen, Qilong;Huo, Keke
    • Molecules and Cells
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    • 제37권9호
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    • pp.691-698
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    • 2014
  • SCYL1-BP1 is thought to function in the p53 pathway through Mdm2 and hPirh2, and mutations in SCYL1-BP1 are associated with premature aging syndromes such as Geroderma Osteodysplasticum; however, these mechanisms are unclear. Here, we report significant alterations in miRNA expression levels when SCYL1-BP1 expression was inhibited by RNA interference in HEK293T cells. We functionally characterized the effects of potential kernel miRNA-target genes by miRNA-target network and protein-protein interaction network analysis. Importantly, we showed the diminished SCYL1-BP1 dramatically reduced the expression levels of EEA1, BMPR2 and BRCA2 in HEK293T cells. Thus, we infer that SCYL1-BP1 plays a critical function in HEK293T cell development and directly regulates miRNA-target genes, including, but not limited to, EEA1, BMPR2, and BRCA2, suggesting a new strategy for investigating the molecular mechanism of SCYL1-BP1.

DNA damage to human genetic disorders with neurodevelopmental defects

  • Lee, Youngsoo;Choi, Inseo;Kim, Jusik;Kim, Keeeun
    • Journal of Genetic Medicine
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    • 제13권1호
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    • pp.1-13
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    • 2016
  • Although some mutations are beneficial and are the driving force behind evolution, it is important to maintain DNA integrity and stability because it contains genetic information. However, in the oxygen-rich environment we live in, the DNA molecule is under constant threat from endogenous or exogenous insults. DNA damage could trigger the DNA damage response (DDR), which involves DNA repair, the regulation of cell cycle checkpoints, and the induction of programmed cell death or senescence. Dysregulation of these physiological responses to DNA damage causes developmental defects, neurological defects, premature aging, infertility, immune system defects, and tumors in humans. Some human syndromes are characterized by unique neurological phenotypes including microcephaly, mental retardation, ataxia, neurodegeneration, and neuropathy, suggesting a direct link between genomic instability resulting from defective DDR and neuropathology. In this review, rare human genetic disorders related to abnormal DDR and damage repair with neural defects will be discussed.

A Lipid-derived Endogenous Inducer of COX-2: a Bridge Between Inflammation and Oxidative Stress

  • Uchida, Koji
    • Molecules and Cells
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    • 제25권3호
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    • pp.347-351
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    • 2008
  • Several lines of evidence indicate that the oxidative modification of protein and the subsequent accumulation of the modified proteins have been found in cells during aging, oxidative stress, and in various pathological states including premature diseases, muscular dystrophy, rheumatoid arthritis, and atherosclerosis. The important agents that give rise to the modification of a protein may be represented by reactive aldehydic intermediates, such as ketoaldehydes, 2-alkenals and 4-hydroxy-2-alkenals. These reactive aldehydes are considered important mediators of cell damage due to their ability to covalently modify biomolecules, which can disrupt important cellular functions and can cause mutations. Furthermore, the adduction of aldehydes to apolipoprotein B in low-density lipoproteins (LDL) has been strongly implicated in the mechanism by which LDL is converted to an atherogenic form that is taken up by macrophages, leading to the formation of foam cells. During the search for an endogenous inducer of cyclooxygenase-2 (COX-2), an inducible isoform responsible for high levels of prostaglandin production during inflammation and immune responses, 4-hydroxy-2-noennal (HNE), one of the most representative lipid peroxidation product, has been identified as the potential inducer of COX-2. In addition, the following study on the molecular mechanism of the COX-2 induction by HNE has unequivocally established that a serum component, which is eventually identified to be denatured LDL, is essential for COX-2 induction. Here I review current understanding of the mechanisms by which HNE in cooperation with the serum component activates gene expression of COX-2.

Lack of Association between the Klotho Gene and COPD

  • Kim, Woo-Jin;Oh, Yeon-Mok;Kim, Tae-Hyung;Lee, Ji-Hyun;Kim, Eun-Kyung;Lee, Jin-Hwa;Lee, Sang-Min;Shin, Tae-Rim;Yoon, Ho-Il;Lim, Seong-Yong;Lee, Sang-Do
    • Tuberculosis and Respiratory Diseases
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    • 제71권4호
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    • pp.254-258
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    • 2011
  • Background: Although the aging process and features of chronic obstructive pulmonary disease (COPD) have several similarities, the relationship between aging and COPD pathogenesis remains incompletely understood. The klotho gene was found to be related to premature aging and emphysematous changes in an animal model. We investigated whether klotho gene polymorphisms are related to COPD susceptibility and emphysema severity. Methods: A total of 219 COPD subjects from the Korean Obstructive Lung Disease Cohort and 305 control subjects were genotyped for two single nucleotide polymorphisms (SNPs) of the klotho gene associated with coronary artery disease. Logistic regression was performed to determine the association of these SNPs with COPD susceptibility and linear regression was performed to investigate their association with emphysema severity in COPD subjects. Results: The mean age of the COPD subjects was 66 years and their mean FEV1 was 1.46 L. There were no associations between either SNP or COPD susceptibility (p=0.6 and 0.2, respectively) and there were no associations with emphysema severity. Conclusion: Genetic polymorphisms of the klotho gene were not associated with COPD in a Korean population.