• Tuberculosis and Respiratory Diseases
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• 제67권2호
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• pp.113-120
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• 2009

Background: Reactive oxygen species (ROS) by oxidative stress may play an important role in the pathogenesis of various chronic diseases such as diabetes mellitus, obesity, hyperlipidemia, hypertension and malignancy that are linked to metabolic syndrome. Oxidative stress has been implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF). We examined the relationship between IPF and presenting factors associated with metabolic disorders. Methods: One hundred fourteen patients who met the current consensus of IPF definition were enrolled from March 2000 to April 2006 in Gil Hospital and Samsung Medical Center in Korea. One hundred thirty-four control subjects without pulmonary diseases were selected from subjects who visited Gil hospital for routine medical examinations, including low-dose chest computed tomography from January 2002 to July 2006. Retrospectively, we analyzed the clinical characteristics, the results of blood examinations, and lung function tests from medical records of both groups. Results: IPF patients and control subjects differed in the prevalence of diabetes mellitus as assessed by univariate analysis. Multivariate analysis demonstrated that diabetes mellitus and obesity were associated with IPF. The adjusted odds ratios for diabetes mellitus were 2.733 (95% confidence interval [CI], 1.282~5.827) and 2.001 (95% [CI], 1.063~3.766) for obesity. The remaining factors tested showed no differences between the patient group and the control. Conclusion: Diabetes mellitus and obesity may be associated with IPF development.

• KSBB Journal
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• 제21권6호
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• pp.444-450
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• 2006

본 연구에서는 새로운 주름개선 소재로서 phytoestrogen의 일종인 lignans를 각각 함유하는 연교추출물을 추출 분리하여 노화와 관련된 생리활성 효과를 확인하였다. Arctigenin과 matairesinol을 각각 함유하는 연교추출물은 처리농도가 증가함에 따라 농도 의존적으로 DPPH와 superoxide radical에 대한 소거효과를 나타내었다. DPPH radical 소거효과에서 arctigenin-rich와 matairesinol-rich는 각각 $IC_{50}$ 값이 $5.747{\mu}g/ml,\;4.450\;{\mu}g/ml$를 나타내었으며, superoxide radical 소거효과에서는 각각 1.634 mg/m1, 542.428 mg/ml로 양성 대조군으로 사용한 BHT보다 우수한 항산화 효과를 보였다. Type I collagen 합성효과도 arctigenin 및 matairesinol을 각각 함유한 연교추출물 그리고 양성 대조군 vitamin C를 $100\;{\mu}g/ml$을 처리하였을 때 각각 10.5, 26.4, 15.7%의 합성율을 보임으로써 vitamin C와 유사하거나 우수한 효과를 나타내었다. 또한, UVA에 의해 발현이 증가되는 MMP-1의 발현저해 효과는 matairesinol을 함유한 연교추출물의 경우 oleanolic acid와 유사한 저해 효과를 보였다. Matairesinol을 함유한 연교추출물을 함유한 크림의 피부 주름개선 효과를 평가하기 위하여, 눈가 주름 부위의 제품 도포 후 피부 주름의 변화와 피부거침 개선 효과를 평가하였다. 연교추출물을 함유한 크림을 약 12주간 도포하였을 경우, 깊은 주름과 총 주름수의 감소효과를 관찰할 수 있었으며, 연교추출물 2%를 적용한 인체 안전성시험에서 무자극으로 판명 되 었다. 본 연구를 통하여 lignans를 각각 함유하는 연교추출물은 항산화 효과와 생체 단백질의 30%를 구성하는 collagen의 합성효과 및 UVA에 의한 MMP-1의 발현저해 효과를 보였다. 인체에 무자극성으로 제품에 적용시 관찰되는 피부 주름개선 효과는 lignans를 각각 함유한 연교추출물을 새로운 주름개선을 위한 천연소재로 이용될 수 있을 것으로 사료된다.

• Journal of Dental Anesthesia and Pain Medicine
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• 제17권1호
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• pp.21-28
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• 2017

Background: The skin consists of tightly connected keratinocytes, and prevents extensive water loss while simultaneously protecting against the entry of microbial pathogens. Excessive cellular levels of reactive oxygen species can induce cell apoptosis and also damage skin integrity. Propofol (2,6-diisopropylphenol) has antioxidant properties. In this study, we investigated how propofol influences intracellular autophagy and apoptotic cell death induced by oxidative stress in human keratinocytes. Method: The following groups were used for experimentation: control, cells were incubated under normoxia (5% $CO_2$, 21% $O_2$, and 74% $N_2$) without propofol; hydrogen peroxide ($H_2O_2$), cells were exposed to $H_2O_2$ ($300{\mu}M$) for 2 h; propofol preconditioning (PPC)/$H_2O_2$, cells pretreated with propofol ($100{\mu}M$) for 2 h were exposed to $H_2O_2$; and 3-methyladenine $(3-MA)/PPC/H_2O_2$, cells pretreated with 3-MA (1 mM) for 1 h and propofol were exposed to $H_2O_2$. Cell viability, apoptosis, and migration capability were evaluated. Relation to autophagy was detected by western blot analysis. Results: Cell viability decreased significantly in the $H_2O_2$ group compared to that in the control group and was improved by propofol preconditioning. Propofol preconditioning effectively decreased $H_2O_2$-induced cell apoptosis and increased cell migration. However, pretreatment with 3-MA inhibited the protective effect of propofol on cell apoptosis. Autophagy was activated in the $PPC/H_2O_2$ group compared to that in the $H_2O_2$ group as demonstrated by western blot analysis and autophagosome staining. Conclusion: The results suggest that propofol preconditioning induces an endogenous cellular protective effect in human keratinocytes against oxidative stress through the activation of signaling pathways related to autophagy.

• Journal of Dental Anesthesia and Pain Medicine
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• 제17권1호
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• pp.37-46
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• 2017

Background: In oxidative stress, reactive oxygen species (ROS) production contributes to cellular dysfunction and initiates the apoptotic cascade. Autophagy is considered the mechanism that decreases ROS concentration and oxidative damage. Propofol shows antioxidant properties, but the mechanisms underlying the effect of propofol preconditioning (PPC) on oxidative injury remain unclear. Therefore, we investigated whether PPC protects against cell damage from hydrogen peroxide ($H_2O_2$)-induced oxidative stress and influences cellular autophagy. Method: COS-7 cells were randomly divided into the following groups: control, cells were incubated in normoxia (5% $CO_2$, 21% $O_2$, and 74% $N_2$) for 24 h without propofol; $H_2O_2$, cells were exposed to $H_2O_2$ ($400{\mu}M$) for 2 h; $PPC+H_2O_2$, cells pretreated with propofol were exposed to $H_2O_2$; and 3-methyladenine $(3-MA)+PPC+H_2O_2$, cells pretreated with 3-MA (1 mM) for 1 h and propofol were exposed to $H_2O_2$. Cell viability was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide thiazolyl blue (MTT) reduction. Apoptosis was determined using Hoechst 33342 staining and fluorescence microscopy. The relationship between PPC and autophagy was detected using western blot analysis. Results: Cell viability decreased more significantly in the $H_2O_2$ group than in the control group, but it was improved by PPC ($100{\mu}M$). Pretreatment with propofol effectively decreased $H_2O_2$-induced COS-7 cell apoptosis. However, pretreatment with 3-MA inhibited the protective effect of propofol during apoptosis. Western blot analysis showed that the level of autophagy-related proteins was higher in the $PPC+H_2O_2$ group than that in the $H_2O_2$ group. Conclusion: PPC has a protective effect on $H_2O_2$-induced COS-7 cell apoptosis, which is mediated by autophagy activation.

• 한국식품영양과학회지
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• 제42권10호
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• pp.1525-1532
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• 2013

말채나무 열수추출물의 항산화 활성을 알아보기 위해 HepG2 세포에 TBHP로 산화 스트레스를 유도한 뒤 말채나무 열수추출물의 세포 보호효과, ROS 생성억제, 지질과산화 억제 및 GSH 생성에 미치는 영향에 대해 살펴보았다. 말채나무 열수추출물은 HepG2 세포에 TBHP로 산화 스트레스를 유도한 뒤 나타나는 세포독성에 대해 농도 의존적으로 유의하게 세포 보호효과를 보였으며, ROS 생성과 과산화물에 대한 지표로서 측정한 MDA도 말채나무 열수추출물에 의해 효과적으로 억제되었다(P<0.05). 또한 항산화 성분으로 생체 내에서 산화 및 환원반응에 중요한 역할을 하며 항산화 효소인 GSH-Px, GST에 전자공여체로 작용하는 GSH의 생성촉진 효능에서도 말채나무 열수추출물은 산화 스트레스로 감소된 GSH의 생성을 농도 의존적으로 촉진시켰다(P<0.05). 산화 스트레스에 의해 활성이 증가된 항산화 효소(CAT, SOD, GSH-Px, GR)도 말채나무 열수추출물의 처리로 감소하는 경향을 보였다. 이러한 결과로 미루어 보아 말채나무 열수 추출물은 인체 내에서 질병과 노화를 일으키는 원인 물질인 활성산소에 대해 강한 항산화 활성을 나타냄에 따라 보다 다양한 형태의 소재로 활용될 수 있을 것으로 생각된다.

• 한국식품영양과학회지
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• 제46권2호
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• pp.161-168
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• 2017

본 연구에서는 산화적 스트레스로 유도한 시신경 세포사멸에 대한 차조기 물 추출물(PFE)의 효과를 확인하였다. Staurosporine으로 분화된 ssdRGC-5 세포에 buthionine과 glutamate(B/G)로 산화적 스트레스를 유도하였으며, LDH release assay, MTT reduction assay를 통하여 PFE가 농도 의존적으로 B/G에 의한 세포사멸을 억제함을 관찰하였다. 세포사멸의 기전을 연구하기 위해 caspase 활성, 세포 내 ROS 생성량, 세포고사 관련 단백질 발현을 관찰한 결과, B/G에 의해 증가한 ROS 생성량, caspase 활성을 PFE가 억제하였고, 세포질로 방출된 cytochrome c와 미토콘드리아로 이동한 Bax도 감소함을 확인하였다. 이상의 결과로부터 차조기는 산화적 스트레스로 유도된 시신경 세포사멸 과정에서 항산화 효과와 미토콘드리아성 세포사멸을 완화함으로써 세포 보호 작용을 나타냄을 확인하였다.

• BMB Reports
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• 제47권10호
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• pp.569-574
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• 2014

Heme oxygenase-1 (HO-1) degrades heme to carbon dioxide, biliverdin, and $Fe^{2+}$, which play important roles in various biochemical processes. In this study, we examined the protective function of HO-1 against oxidative stress in SH-SY5Y cells and in a Parkinson's disease mouse model. Western blot and fluorescence microscopy analysis demonstrated that PEP-1-HO-1, fused with a PEP-1 peptide can cross the cellular membranes of human neuroblastoma SH-SY5Y cells. In addition, the transduced PEP-1-HO-1 inhibited generation of reactive oxygen species (ROS) and cell death caused by 1-methyl-4-phenylpyridinium ion ($MPP^+$). In contrast, HO-1, which has no ability to transduce into SH-SY5Y cells, failed to reduce $MPP^+$-induced cellular toxicity and ROS production. Furthermore, intraperitoneal injected PEP-1-HO-1 crossed the blood-brain barrier in mouse brains. In a PD mouse model, PEP-1-HO-1 significantly protected against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced toxicity and dopaminergic neuronal death. Therefore, PEP-1-HO-1 could be a useful agent in treating oxidative stress induced ailments including PD.

• BMB Reports
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• 제53권11호
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• pp.582-587
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• 2020

It is well known that oxidative stress participates in neuronal cell death caused production of reactive oxygen species (ROS). The increased ROS is a major contributor to the development of ischemic injury. Indoleamine 2,3-dioxygenase 1 (IDO-1) is involved in the kynurenine pathway in tryptophan metabolism and plays a role as an anti-oxidant. However, whether IDO-1 would inhibit hippocampal cell death is poorly known. Therefore, we explored the effects of cell permeable Tat-IDO-1 protein against oxidative stress-induced HT-22 cells and in a cerebral ischemia/reperfusion injury model. Transduced Tat-IDO-1 reduced cell death, ROS production, and DNA fragmentation and inhibited mitogen-activated protein kinases (MAPKs) activation in H₂O₂ exposed HT-22 cells. In the cerebral ischemia/reperfusion injury model, Tat-IDO-1 transduced into the brain and passing by means of the blood-brain barrier (BBB) significantly prevented hippocampal neuronal cell death. These results suggest that Tat-IDO-1 may present an alternative strategy to improve from the ischemic injury.

• Fisheries and Aquatic Sciences
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• 제20권4호
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• pp.6.1-6.8
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• 2017

The objective of this research was to study the effect of astaxanthin (AST) on growth performance and antioxidant capacity in golden pompano (Trachinotus ovatus) both in vivo and in vitro. In the in vivo study, two diets were formulated with or without astaxanthin supplementation (D1 and D2; 0 and 200 mg/kg) to feed fish for 6 weeks. In the in vitro study, cells from hepatopancreas of golden pompano were isolated and four treatments with or without astaxanthin and $H_2O_2$ supplementation were applied (control group: without both astaxanthin and $H_2O_2$ treated; $H_2O_2$ group: just with $H_2O_2$ treated; $H_2O_2$ + AST group: with both astaxanthin and $H_2O_2$treated; AST group: just with AST treated). Results of the in vivo study showed that weight gain (WG) and special growth rate (SGR) significantly increased with astaxanthin supplemented (P < 0.05). Feed conversion ratio (FCR) of fish fed D2 diet was significantly lower than that of fish fed D1 diet (P < 0.05). Hepatic total antioxidant capacity (T-AOC) and the reduced glutathione (GSH) of golden pompano fed D2 diet were significant higher than those of fish fed D1 diet (P < 0.05). Superoxide dismutase (SOD) was significantly declined as astaxanthin was supplemented (P < 0.05). Results of the in vitro study showed that the cell viability of $H_2O_2$ group was 52.37% compared to the control group, and it was significantly elevated to 84.18% by astaxanthin supplementation ($H_2O_2$ + AST group) (P < 0.05). The total antioxidant capacity (T-AOC) and the reduced glutathione (GSH) of cell were significant decreased by oxidative stress from $H_2O_2$ (P < 0.05), but it could be raised by astaxanthin supplementation ($H_2O_2$ vs $H_2O_2$ + AST), and the malondialdehyde (MDA) was significant higher in $H_2O_2$ group (P < 0.05) and astaxanthin supplementation could alleviate the cells from lipid peroxidation injury. In conclusion, dietary astaxanthin supplementation can improve the growth performance of golden pompano. Moreover, astaxanthin can improve the golden pompano hepatic antioxidant capacity both in vivo and in vitro study by eliminating the reactive oxygen species.

• BMB Reports
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• 제48권11호
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• pp.618-623
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• 2015

FK506 binding protein 12 (FK506BP) is a small peptide with a single FK506BP domain that is involved in suppression of immune response and reactive oxygen species. FK506BP has emerged as a potential drug target for several inflammatory diseases. Here, we examined the protective effects of directly applied cell permeable FK506BP (PEP-1-FK506BP) on corneal alkali burn injury (CAI). In the cornea, there was a significant decrease in the number of cells expressing pro-inflammation, apoptotic, and angiogenic factors such as TNF-α, COX-2, and VEGF. Both corneal opacity and corneal neovascularization (CNV) were significantly decreased in the PEP-1-FK506BP treated group. Our results showed that PEP-1-FK506BP can significantly inhibit alkali burn-induced corneal inflammation in rats, possibly by accelerating corneal wound healing and by reducing the production of angiogenic factors and inflammatory cytokines. These results suggest that PEP-1-FK506BP may be a potential therapeutic agent for CAI.