• Tuberculosis and Respiratory Diseases
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• v.67 no.2
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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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• v.21 no.6 s.101
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• pp.444-450
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• 2006

Skin anti-aging effect of Forsythia viridissima L. extract was evaluated by using antioxidant assay, expression of type I procollagen, and UVA-induced matrix metalloproteinase-1 in human dermal fibroblasts. Matairesinol-rich Forsythia viridissima L. extract was showed the scavenging activity of radicals and reactive oxygen species with the $IC_{50}$ values of $4.50\;{\mu}m/ml$ against 1,1-diphenyl-2-picrylhydrazly radical and $542.43\;{mu}m/ml$ against superoxide radicals in the xanthine/xanthine oxidase system, respectively. The type I procollagen was increased 33.76% by treatment with matairesinol-rich Forsythia viridissima L. extract, and UVA-induced MMP-1 was reduced 35.78% in a dose dependent manner. In the human skin irritation test, 2% matairesinol-rich Forsythia viridissima L. extract did not show any adverse effect. Also, the clinical study indicated that a cream group treated with 0.2% matairesinol-rich Forsythia viridissima L. extract significantly reduced skin wrinkles, as compared with a non-treated cream group (p < 0.05). These results suggest that Forsythia viridissima L. extract may be useful as a potential source of functional anti-aging cosmetics.

• Journal of Dental Anesthesia and Pain Medicine
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• v.17 no.1
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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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• v.17 no.1
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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.

• Journal of the Korean Society of Food Science and Nutrition
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• v.42 no.10
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• pp.1525-1532
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• 2013

The objective of this study was to investigate the effect of hot water extract from Cornus walteri Wanger (CWE) on tert-butyl hydroperoxide (TBHP)-induced oxidative stress in HepG2 cells. Generation of reactive oxygen species (ROS), concentrations of cellular lipid peroxidation products and reduced glutathione, and antioxidant enzyme activity were used as biomakers of cellular oxidative status. Cells pretreated with CWE (25~200 ${\mu}g/mL$) showed an increased resistance to oxidative stress in a dose-dependent manner, as revealed by a higher percentage of surviving cells compared to control cells. ROS generation induced by TBHP was significantly reduced when cells were pretreated with 200 ${\mu}g/mL$ CWE for 4 h. Pretreatment with CWE (5~50 ${\mu}g/mL$) prevented the decrease in reduced glutathione and the increase in malondialdehyde and ROS evoked by TBHP in HepG2 cells. Finally, CWE pretreatments prevented the significant increase of glutathione peroxidase, catalase, glutathione reductase, and superoxide dismutase activities induced by TBHP. These results show that CWE has significant protective ability against a TBHP-induced oxidative insult and that the modulation of antioxidant enzymes by CWE may have an important antioxidant effect on TBHP-induced oxidative stress in HepG2 cells.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.2
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• pp.161-168
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• 2017

In this study, we examined the effect of Perilla frutescens extract (PFE) on oxidative stress-induced cell death in RGC-5 cell lines. Staurosporine-differentiated RGC-5 (ssdRGC-5) cells obtained by treating RGC-5 cells with $1{\mu}M$ staurosporine were incubated with PFE for 30 min and then exposed to buthionine sulfoximine plus glutamate (B/G) for 20 h. Cell death was detected using lactate dehydrogenase release assay and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction assay. To investigate the mechanism underlying cell death, we determined caspase-3 activity, level of reactive oxygen species (ROS) formation, and expression levels of cytoplasmic cytochrome c and mitochondrial Bax. Treatment of ssdRGC-5 cells with B/G increased intracellular ROS and induced apoptosis with increasing caspase-3 activity. PFE rescued ssdRGC-5 cells from oxidative stress-induced cell death by inhibiting intracellular ROS production and caspase-3 activation and regulating apoptosis-related proteins such as cytochrome c and Bax. These findings suggest that PFE may have a beneficial neuroprotective effect against oxidative stress-induced apoptotic death in ssdRGC-5 cells.

• BMB Reports
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• v.47 no.10
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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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• v.53 no.11
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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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• v.20 no.4
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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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• v.48 no.11
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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.