• Journal of Applied Biological Chemistry
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• v.63 no.4
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• pp.357-363
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• 2020

Oxidative stress caused by the overproduction of reactive oxygen species (ROS) is known as an etiology of neurodegenerative diseases. Populus tomentiglandulosa (PT), a member of the Salicaceae family, is widely grown in Korea and has been reported to exert protective effects on cerebral ischemia by attenuating of oxidative stress and neuronal damage. In the present study, we investigated the antioxidant activity and neuroprotective effects of an ethanol extract and four fractions [n-butanol, ethyl acetate (EtOAc), chloroform, and n-hexane] of PT under in vitro and cellular systems. The extract and four fractions of PT showed 1,1-diphenyl-2-picrylhydrazyl (DPPH), •OH, and O2- radical scavenging activities in a dose-dependent manner. In particular, the EtOAc fraction of PT had the strongest DPPH, •OH, and O2- radical scavenging activities among the extract and other fractions. Therefore, we further investigated the neuroprotective effect of the EtOAc fraction of PT against oxidative stress in H2O2-induced SH-SY5Y cells. Treatment with H2O2 significantly decreased cell viability and lactate dehydrogenase (LDH) release, and it also increased the ROS levels compared to the normal group. However, treatment with the EtOAc fraction of PT significantly increased cell viability. Moreover, the EtOAc fraction of PT-treated group significantly suppressed ROS production and LDH release compared to the H2O2-induced control group. In conclusion, our findings indicated that PT had in vitro antioxidant activity and neuroprotective effects against oxidative stress. Therefore, PT could be used as a natural agent for protection against oxidative stress.

• Journal of Ginseng Research
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• v.45 no.4
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• pp.473-481
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• 2021

Background: Mitochondrial dysfunction is one of the significant reasons for Alzheimer's disease (AD). Ginsenosides, natural molecules extracted from Panax ginseng, have been demonstrated to exert essential neuroprotective functions, which can ascribe to its anti-oxidative effect, enhancing central metabolism and improving mitochondrial function. However, a comprehensive analysis of cellular mitochondrial bioenergetics after ginsenoside treatment under Aβ-oxidative stress is missing. Methods: The antioxidant activities of ginsenoside Rb₁, Rd, Re, Rg₁ were compared by measuring the cell survival and reactive oxygen species (ROS) formation. Next, the protective effects of ginsenosides of mitochondrial bioenergetics were examined by measuring oxygen consumption rate (OCR) in PC12 cells under Aβ-oxidative stress with an extracellular flux analyzer. Meanwhile, mitochondrial membrane potential (MMP) and mitochondrial dynamics were evaluated by confocal laser scanning microscopy. Results: Ginsenoside Rg₁ possessed the strongest anti-oxidative property, and which therefore provided the best protective function to PC12 cells under the Aβ oxidative stress by increasing ATP production to 3 folds, spare capacity to 2 folds, maximal respiration to 2 folds and non-mitochondrial respiration to 1.5 folds, as compared to Aβ cell model. Furthermore, ginsenoside Rg1 enhanced MMP and mitochondrial interconnectivity, and simultaneously reduced mitochondrial circularity. Conclusion: In the present study, these results demonstrated that ginsenoside Rg₁ could be the best natural compound, as compared with other ginsenosides, by modulating the OCR of cultured PC12 cells during oxidative phosphorylation, in regulating MMP and in improving mitochondria dynamics under Aβ-induced oxidative stress.

• Journal of Ginseng Research
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• v.46 no.3
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• pp.496-504
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• 2022

Background: Cigarette smoke (CS) is considered a principal cause of chronic obstructive pulmonary disease (COPD) and is associated with mucus hypersecretion and airway inflammation. Ginsenoside compound K (CK), a product of ginsenoside metabolism, has various biological activities. Studies on the effects of CK for the treatment of COPD and mucus hypersecretion, including the underlying signaling mechanism, have not yet been conducted. Methods: To study the protective effects and molecular mechanism of CK, phorbol 12-myristate 13-acetate (PMA)-induced human airway epithelial (NCI-H292) cells were used as a cellular model of airway inflammation. An experimental mouse COPD model was also established via CS inhalation and intranasal administration of lipopolysaccharide. Mucin 5AC (MUC5AC), monocyte chemoattractant protein-1, tumor necrosis factor-α (TNF-α), and interleukin-6 secretion, as well as elastase activity and reactive oxygen species production, were determined through enzyme-linked immunosorbent assay. Inflammatory cell influx and mucus secretion in mouse lung tissues were estimated using hematoxylin and eosin and periodic acid-schiff staining, respectively. PKCδ and its downstream signaling molecules were analyzed via western blotting. Results: CK prevented the secretion of MUC5AC and TNF-α in PMA-stimulated NCI-H292 cells and exhibited a protective effect in COPD mice via the suppression of inflammatory mediators and mucus secretion. These effects were accompanied by an inactivation of PKCδ and related signaling in vitro and in vivo. Conclusion: CK suppressed pulmonary inflammation and mucus secretion in COPD mouse model through PKC regulation, highlighting the compound's potential as a useful adjuvant in the prevention and treatment of COPD.

• Journal of Veterinary Science
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• v.25 no.1
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• pp.4.1-4.14
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• 2024

Background: Lawsonia intracellularis is the causative agent of proliferative enteropathy and is associated with several outbreaks, causing substantial economic loss to the porcine industry. Objectives: In this study, we focused on demonstrating the protective effect in the mouse model through the immunological bases of two vaccine strains against porcine proliferative enteritis. Methods: We used live-attenuated Salmonella Typhimurium (ST) secreting two selected immunogenic LI antigens (Lawsonia autotransporter A epitopes and flagellin [FliC]-peptidoglycan-associated lipoprotein-FliC) as the vaccine carrier. The constructs were cloned into a Salmonella expression vector (pJHL65) and transformed into the ST strain (JOL912). The expression of immunogenic proteins within Salmonella was evaluated via immunoblotting. Results: Immunizing BALB/c mice orally and subcutaneously induced high levels of LI-specific systemic immunoglobulin G and mucosal secretory immunoglobulin A. In immunized mice, there was significant upregulation of interferon-γ and interleukin-4 cytokine mRNA and an increase in the subpopulations of cluster of differentiation (CD) 4⁺ and CD 8⁺ T lymphocytes upon splenocytes re-stimulation with LI antigens. We observed significant protection in C57BL/6 mice against challenge with 10^6.9 times the median tissue culture infectious dose of LI or 2 × 10⁹ colony-forming units of the virulent ST strain. Immunizing mice with either individual vaccine strains or co-mixture inhibited bacterial proliferation, with a marked reduction in the percentage of mice shedding Lawsonia in their feces. Conclusions: Salmonella-mediated LI gene delivery induces robust humoral and cellular immune reactions, leading to significant protection against LI and salmonellosis.

• Journal of Applied Biological Chemistry
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• v.61 no.2
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• pp.109-117
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• 2018

Recently, cancer incidence in modern society is increasing sharply. DNA damage is caused by intrinsic or extrinsic factors in the human body, cells protect themselves by defense mechanism against DNA damage. Also, Aberrant DNA and deficient DNA repair are closely associated with various diseases, including aging and cancer. Researchers are interested in search for proper materials to inhibition for DNA damage. As knew the side effects of synthetic antioxidant, some researches have been conducted about cancer prevention materials derived from nature. Root of Smilax china, in Liliaceae, is used detoxification and tumor treatments traditionally. However, studies on the inhibitory effect of DNA damage haven't progressed. In this study, antioxidant activity and protective effects on oxidative DNA damage of S. china root were confirmed, relationship between those activities and contents of phenolic compounds in plants were established. S. china root effectively removed 1,1-diphenyl-2-picryl-hydrazyl radicals and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid radicals. The quantification and identification of phenolic compounds were confirmed by high performance liquid chromatography analysis, its antioxidant activity was associated with some phenolic compounds. In addition, protective effects against hydroxyl radicals and ferrous ion-induced oxidative DNA damage were confirmed in plasmid DNA. In the cellular levels, S. china root suppressed the expression of ${\gamma}$-H2AX and p53 protein in NIH 3T3. Besides, S. china root suppressed H2AX and p53 mRNA levels. In conclusion, S. china root had the effect on DNA protection and antioxidant.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.5
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• pp.283-289
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• 2005

Endothelium, particularly pulmonary endothelium, is predisposed to injury by reactive oxygen species (ROS) and their derivatives. Heme oxygenase (HO) has been demonstrated to provide cytoprotective effects in models of oxidant-induced cellular and tissue injuries. In the present study, we investigated the effects of YS 49 against oxidant [tert-butylhydroperoxide (TBH)]-induced injury using cultured sheep pulmonary artery endothelial cells (SPAECs). The viability of SPAECs was determined by quantifying reduction of a fluorogenic indicator Alamar blue. We found that TBH decreased cell viability in a timeand concentration-dependent manner. YS 49 concentration- and time-dependently increased HO-1 induction on SPAECs. As expected, YS 49 significantly decreased the TBH-induced cellular injury. In the presence of zinc protophorphyrin, HO-1 inhibitor, effect of YS 49 was significantly inhibited, indicating that HO-1 plays a protective role for YS 49. Furthermore, YS 49 showed free radical scavenging activity as evidenced by 1,1-diphenyl-2-picrylhydrazyl (DPPH) and inhibition of lipid peroxidation. However, YS 49 did not inhibit apoptosis induced by lipopolysaccharide (LPS) in SPAECs. Taken together, HO-1 induction along with strong antioxidant action of YS 49 may be responsible for inhibition of TBH-induced injury in SPAECs.

• Toxicological Research
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• v.24 no.4
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• pp.245-251
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• 2008

Dietary restriction (DR) is the most efficacious intervention for retarding the deleterious effects of aging. DR increases longevity, decreases the occurrence and severity of age-related diseases, and retards the physiological decline associated with aging. The beneficial effects of DR have been mostly studied in non-neuronal tissues. However, several studies have showed that DR attenuate neuronal loss after several different insults including exposure to kainate, ischemia, and MPTP. Moreover, administration of the non-metabolizable glucose analog 2-deoxy-D-glucose (2DG) could mimic the neuroprotective effect of DR in rodent, presumably by limiting glucose availability at the cellular level. Based on the studies of chemically induced DR, it has been proposed that the mechanism whereby DR and 2DG protect neurons is largely mediated by stress response proteins such as HSP70 and GRP78 which are increased in neurons of rats and mice fed a DR regimen. In addition, DR, as mild metabolic stress, could lead to the increased activity in neuronal circuits and thus induce expression of neurotrophic factors. Interestingly, such increased neuronal activities also enhance neurogenesis in the brains of adult rodents. In this review, we focus on what is known regarding molecular mechanisms of the protective role of DR in neurodegenerative diseases and aging process. Also, we propose that DR is a mild cellular stress that stimulates production of neurotrophic factors, which are major regulators of neuronal survival, as well as neurogenesis in adult brain.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.4
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• pp.1649-1654
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• 2016

Tea derived from the leaves and buds of Camellia sinensis (Theaceae) is consumed worldwide. Green tea contains various components with specific health-promoting effects, and is believed to exert protective effects against diseases including cancer, diabetes and hepatitis, as well as obesity. Of the various tea components, the polyphenol catechins have been the subject of extensive investigation and among the catechins, (-)-epigallocatechin gallate has the strongest bioactivity in most cases. Our research group has postulated that hepatocyte nuclear factor-$4{\alpha}$, sterol regulatory element-binding proteins, and tumor necrosis factor-${\alpha}$ are targets of green tea constituents including (-)-epigallocatechin gallate for their anti-diabetes, anti-obesity, and anti-hepatitis effects, respectively. Published papers were reviewed to determine whether the observed changes in these factors can be correlated with anti-cancer effects of green tea. Two major action mechanisms of (-)-epigallocatechin gallate have been proposed; one associated with its anti-oxidative properties and the other with its pro-oxidative activity. When reactive oxygen species are assumed to be involved, our findings that (-)-epigallocatechin gallate downregulated hepatocyte nuclear factor-$4{\alpha}$, sterol regulatory element-binding proteins, and tumor necrosis factor-${\alpha}$ may explain the anti-cancer effect of green tea as well. However, further studies are required to elucidate which determinant directs (-)-epigallocatechin gallate action as an anti-oxidant or a pro-oxidant for favorable activity.

• Fisheries and Aquatic Sciences
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• v.16 no.3
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• pp.149-158
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• 2013

We demonstrate enhanced growth, innate immunity and protection against hydrogen peroxide ($H_2O_2$)-induced protein oxidation and cellular DNA damage in olive flounder Paralichthys olivaceus fed a chitosan-coated moist pallet (MP) diet. A chitosan-based biopolymer coated MP as the experimental diet and a non-coated MP (control) was fed to olive flounder fish. Growth, including the average weight gain (g/fish), weight gain (%) and feed intake (g) of the fish group fed a chitosan-coated MP diet increased significantly. The survival rate was reported as 100% throughout the experimental period. Immunological parameters indicated higher mucus lysozyme activity and significantly higher fish skin mucus total protein content was observed in fish fed the chitosan-coated MP diet compared to the control. A blood plasma analysis revealed attenuation of cellular DNA and protein oxidative damage caused by $H_2O_2$-induced oxidative stress in the fish fed the chitosan-coated MP diet compared to the control group. Moreover, blood serum biochemical analysis revealed health-promoting effects, including significantly higher hemoglobin and total cholesterol levels in the fish fed the chitosan-coated MP diet compared to the control group. In conclusion, growth, innate immunity and protection against oxidative stresses were improved by feeding of the chitosan-coated MP diet to olive flounder reared in aquaculture.

• Korean Journal of Agricultural Science
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• v.47 no.3
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• pp.497-508
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• 2020

In this study, we investigated the protective effects of 'Donganme' (Sorghum bicolor L. Moench) against oxidative stress under in vitro conditions and in a cellular system using C6 glial cells. The radical scavenging activities were observed using the substrates 1,1-diphenyl-2-picrylhydrazyl (DPPH) and hydroxyl (•OH) radicals. The Donganme extract had an •OH radical scavenging activity of 82.66% at a concentration of 100 ㎍·mL^-1. Additionally, when DPPH was used as the substrate, the Donganme extract exhibited a strong radical scavenging activity in a concentration-dependent manner with an IC₅₀ value of 28.56 ㎍·mL^-1. Furthermore, treating C6 glial cells with hydrogen peroxide (H₂O₂) reduced the cell viability and generated reactive of oxygen species (ROS) and lactate dehydrogenase (LDH) compared to the normal levels, indicating that H₂O₂ induced oxidative stress. However, Donganme extracts increased the cell viability and inhibited ROS and LDH production against oxidative stress by H₂O₂ in the C6 glial cells. In particular, it showed effective cell protection with the cell viability, ROS production, and LDH release at 83.50, 88.06, and 14.87%, respectively, which were lower than the control or similar to the normal levels even at a low concentration of 100 ㎍·mL^-1. The present study suggests that the Donganme extract was effective in protecting against oxidative stress in C6 glial cells through its antioxidant activity. Thus, Donganme could be a promising therapeutic agent for neurodegenerative diseases due to oxidative stress.