Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.8
7.0
Journals
Antioxidants
Special Issues
Oxidative Damage in Korean Medicine
share announcement

Oxidative Damage in Korean Medicine

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 19544

Special Issue Editor

Dr. Gunhyuk Park

E-Mail Website
Guest Editor
Herbal Medicine Resources Research Center, Korea Institute of Oriental Medicine, Daejeon 58245, Jeollanam-do, Republic of Korea
Interests: oxidative stress; redox signaling; nuclear factor erythroid 2-related factor 2 (NRF2); neurodegenerative disease; skin disease; HPA axis; skin–brain axis; supplements and functional foods
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Interest in antioxidants has highly increased over the last few decades due to their beneficial effects in the prevention of degenerative diseases and in the processes associated with aging. Reactive oxygen species (ROS), where the main free radicals are framed, are highly reactive molecules that are constantly produced in biological reactions, whose excess is usually neutralized by a battery of defense mechanisms of the living organisms, including enzymes, vitamins, and a series of small antioxidant molecules. Depleted antioxidant defenses or overproduction of ROS can lead to oxidative stress, increasing the likelihood of damage to biological macromolecules, such as proteins, DNA and lipids. This damage is implicated in the severity of chronic diseases and, in that situation, dietary antioxidants gain special importance.

Modernized Korean medicine currently utilizes cutting-edge techniques of orthodox medicine, though it is rooted in the Donguibogam, one of the best Korean medical classics written in 1610 and enlisted in the Memory of the Word by UNESCO in 2009. Currently, many researchers are working to develop treatments for the disease through modernizing Donguibogam and scientific evidence. In particular, research on the applicability of antioxidant and antiaging effects is being conducted intensively. Therefore, scientific research on antioxidants in Korean medicine or Korean herbal medicine is currently of great interest.

This Special Issue will focus on both observational, molecular, and mechanistic studies investigating the impact of upregulating antioxidant effects toward health recovery and treatment of diseases using Korean medicine.

Dr. Gunhyuk Park
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Aging
  • Anti-oxidants
  • Korean medicine
  • Inflammation
  • Redox biology.

Published Papers (7 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Editorial

Jump to: Research

3 pages, 177 KiB  
Editorial
Oxidative Damage in Korean Medicine
by Gunhyuk Park
Antioxidants 2022, 11(3), 600; https://doi.org/10.3390/antiox11030600 - 21 Mar 2022
Cited by 1 | Viewed by 1643
Abstract
Korean medicine originated in ancient and prehistoric times, as evidenced by the discovery of stone and bone needles in the North Hamgyeong Province, dating back to 3000 BC [...] Full article
(This article belongs to the Special Issue Oxidative Damage in Korean Medicine)

Research

Jump to: Editorial

16 pages, 2546 KiB  
Article
Insamgobonhwan Protects Neuronal Cells from Lipid ROS and Improves Deficient Cognitive Function
by Ji Hye Yang, Cong Duc Nguyen, Gihyun Lee and Chang-Su Na
Antioxidants 2022, 11(2), 295; https://doi.org/10.3390/antiox11020295 - 31 Jan 2022
Cited by 9 | Viewed by 2818
Abstract
Iron is an essential element in the central nervous system that is involved in many of its important biological processes, such as oxygen transportation, myelin production, and neurotransmitter synthesis. Previous studies have observed the selective accumulation of iron in Aβ aggregates and neurofibrillary [...] Read more.
Iron is an essential element in the central nervous system that is involved in many of its important biological processes, such as oxygen transportation, myelin production, and neurotransmitter synthesis. Previous studies have observed the selective accumulation of iron in Aβ aggregates and neurofibrillary tangles in the brains of patients with Alzheimer’s disease, and excess of this accumulation is associated with accelerated cognitive decline in Alzheimer’s patients. Emerging evidence suggests that ferroptosis, cell death due to iron accumulation, is a potential therapeutic target for treating Alzheimer’s disease. Insamgobonhwan (GBH) is a well-regarded traditional medicine from Donguibogam that possess antioxidant properties and has been suggested to slow the aging process. However, the neuroprotective role of GBH against lipid peroxidation-induced ferroptosis and its positive cognitive effects remain unexplored. Here, we investigated the ability of GBH to protect against RSL3-induced ferroptosis in vitro and to suppress amyloid-β-induced cognitive impairment in vivo. First, we treated HT22 cells with RSL3 to induce ferroptosis, which is an inhibitor of glutathione peroxidase 4 (GPX4) and induces lethal lipid hydroperoxide accumulation, reactive oxygen species (ROS) production, and ferroptotic cell death. GBH treatment inhibited cell death and lipid peroxidation, which were increased by RSL3 administration. In addition, GBH restored the expression of ferroptosis marker proteins, such as GPX4, HO-1 and COX-2, which were altered by RSL3. Next, we examined whether the protective ability of GBH in cells was reproduced in animals. We concluded that GBH treatment inhibited Aβ-induced lipid peroxidation and improved Aβ-induced cognitive impairment in mice. Full article
(This article belongs to the Special Issue Oxidative Damage in Korean Medicine)
►▼ Show Figures

Figure 1

16 pages, 3614 KiB  
Article
Hydrangea macrophylla and Thunberginol C Attenuate Stress-Induced Anxiety in Mice
by Jihye Lee, Huiyoung Kwon, Eunbi Cho, Jieun Jeon, In-Kyu Lee, Wan-Seob Cho, Se Jin Park, Seungheon Lee, Dong Hyun Kim and Ji Wook Jung
Antioxidants 2022, 11(2), 234; https://doi.org/10.3390/antiox11020234 - 26 Jan 2022
Cited by 3 | Viewed by 2706
Abstract
Stress is an important neurological input for successful life. However, chronic stress and stress hormones could be a cause of various neurological disorders including anxiety disorders. Therefore, there have been many efforts to find effective materials for curing stress-induced neurological disorders. In this [...] Read more.
Stress is an important neurological input for successful life. However, chronic stress and stress hormones could be a cause of various neurological disorders including anxiety disorders. Therefore, there have been many efforts to find effective materials for curing stress-induced neurological disorders. In this study, we examined the effect of Hydrangea macrophylla (HM) on corticosterone-induced neurotoxicity, stress-induced anxiety in mice and suggested a possible active ingredient of HM. HM protected cortical neurons against neurotoxicity of corticosterone (CORT), a stress hormone. HM also blocked CORT-induced hippocampal synaptic deficit via regulating Akt signaling. Oral administration of HM improved chronic restraint stress-induced anxiety in Elevated Plus maze test along with reduction of plasma corticosterone and TNF-α levels. Moreover, HM reduced stress-induced neuroinflammation and oxidative stress. Thunberginol C, an active ingredient of HM, also prevented CORT-induced neuronal cell death and restraint stress-induced anxiety. Moreover, thunberginol C reduced plasma TNF-α level and neuroinflammation and oxidative stress. Collectively, HM could be a good candidate for preventing stress-induced neurological disorders and thunberginol C may be an active ingredient of HM for this purpose. Full article
(This article belongs to the Special Issue Oxidative Damage in Korean Medicine)
►▼ Show Figures

Figure 1

14 pages, 3247 KiB  
Article
Antioxidative and Analgesic Effects of Naringin through Selective Inhibition of Transient Receptor Potential Vanilloid Member 1
by Sanung Eom, Bo-Bae Lee, Shinhui Lee, Youngseo Park, Hye Duck Yeom, Tae-Hwan Kim, Seung-Hee Nam and Junho H. Lee
Antioxidants 2022, 11(1), 64; https://doi.org/10.3390/antiox11010064 - 28 Dec 2021
Cited by 13 | Viewed by 1707
Abstract
Transient receptor potential vanilloid member 1 (TRPV1) is activated in response to capsaicin, protons, temperature, and free reactive oxygen species (ROS) released from inflammatory molecules after exposure to harmful stimuli. The expression level of TRPV1 is elevated in the dorsal root ganglion, and [...] Read more.
Transient receptor potential vanilloid member 1 (TRPV1) is activated in response to capsaicin, protons, temperature, and free reactive oxygen species (ROS) released from inflammatory molecules after exposure to harmful stimuli. The expression level of TRPV1 is elevated in the dorsal root ganglion, and its activation through capsaicin and ROS mediates neuropathic pain in mice. Its expression is high in peripheral and central nervous systems. Although pain is a response evolved for survival, many studies have been conducted to develop analgesics, but no clear results have been reported. Here, we found that naringin selectively inhibited capsaicin-stimulated inward currents in Xenopus oocytes using a two-electrode voltage clamp. The results of this study showed that naringin has an IC50 value of 33.3 μM on TRPV1. The amino acid residues D471 and N628 of TRPV1 were involved in its binding to naringin. Our study bridged the gap between the pain suppression effect of TRPV1 and the preventive effect of naringin on neuropathic pain and oxidation. Naringin had the same characteristics as a model selective antagonist, which is claimed to be ideal for the development of analgesics targeting TRPV1. Thus, this study suggests the applicability of naringin as a novel analgesic candidate through antioxidative and analgesic effects of naringin. Full article
(This article belongs to the Special Issue Oxidative Damage in Korean Medicine)
►▼ Show Figures

Figure 1

21 pages, 4659 KiB  
Article
Crude Saponin from Platycodon grandiflorum Attenuates Aβ-Induced Neurotoxicity via Antioxidant, Anti-Inflammatory and Anti-Apoptotic Signaling Pathways
by Yun-Jeong Ji, Sujin Kim, Jwa-Jin Kim, Gwi Yeong Jang, Minho Moon and Hyung Don Kim
Antioxidants 2021, 10(12), 1968; https://doi.org/10.3390/antiox10121968 - 09 Dec 2021
Cited by 8 | Viewed by 3257
Abstract
Although Platycodon grandiflorum saponins exhibit many beneficial biological effects in various diseases and conditions, how they protect nerve cells against neurodegenerative diseases and Alzheimer’s disease (AD) pathology is unknown. We investigated whether P. grandiflorum crude saponin (PGS) protects neurons from neurodegeneration caused by [...] Read more.
Although Platycodon grandiflorum saponins exhibit many beneficial biological effects in various diseases and conditions, how they protect nerve cells against neurodegenerative diseases and Alzheimer’s disease (AD) pathology is unknown. We investigated whether P. grandiflorum crude saponin (PGS) protects neurons from neurodegeneration caused by amyloid beta (Aβ)-induced oxidative stress. Hippocampal neuron HT-22 cells were used in the in vitro experiment, and AD mice (5XFAD mice) were used as the in vivo model. Intracellular reactive oxygen species (ROS) was stained with DCF-DA and assessed using fluorescence microscopy. To elucidate the mechanism underlying neuroprotection, intracellular protein levels were assessed by western blotting. In 5XFAD mice, an animal model of AD, nerve damage recovery due to the induction of Aβ toxicity was evaluated by histological analysis. PGS attenuates Aβ-induced neurotoxicity by inhibiting Aβ-induced reactive oxygen species (ROS) production and apoptosis in HT-22 cells. Furthermore, PGS upregulated Nrf2-mediated antioxidant signaling and downregulated NF-κB-mediated inflammatory signaling. Additionally, PGS inhibited apoptosis by regulating the expression of apoptosis-associated proteins. In addition, PGS ameliorated Aβ-mediated pathologies, leading to AD-associated cognitive decline. Conclusions: Taken together, these findings suggest that PGS inhibits Aβ accumulation in the subiculum and cerebral cortex and attenuates Aβ toxicity-induced nerve damage in vitro and in vivo. Therefore, PGS is a resource for developing AD therapeutics. Full article
(This article belongs to the Special Issue Oxidative Damage in Korean Medicine)
►▼ Show Figures

Figure 1

17 pages, 4212 KiB  
Article
Mentha arvensis Essential Oil Exerts Anti-Inflammatory in LPS-Stimulated Inflammatory Responses via Inhibition of ERK/NF-κB Signaling Pathway and Anti-Atopic Dermatitis-like Effects in 2,4-Dinitrochlorobezene-Induced BALB/c Mice
by So-Yeon Kim, Sang-Deok Han, Minju Kim, Tamanna Jahan Mony, Eun-Seok Lee, Kyeong-Min Kim, Seung-Hyuk Choi, Sun Hee Hong, Ji Woong Choi and Se Jin Park
Antioxidants 2021, 10(12), 1941; https://doi.org/10.3390/antiox10121941 - 03 Dec 2021
Cited by 26 | Viewed by 4409
Abstract
The mechanism of atopic dermatitis (AD) is modulated by the release of cytokines and chemokines through the mitogen-activated protein kinase (MAPK)/nuclear factor-kappa B (NF-κB) signaling pathway. Topical steroids are used to treat AD, but some people need safer anti-inflammatory drugs to avoid side [...] Read more.
The mechanism of atopic dermatitis (AD) is modulated by the release of cytokines and chemokines through the mitogen-activated protein kinase (MAPK)/nuclear factor-kappa B (NF-κB) signaling pathway. Topical steroids are used to treat AD, but some people need safer anti-inflammatory drugs to avoid side effects. Mentha arvensis has been used as a herbal plant with medicinal properties, but its anti-inflammatory effects have not been elucidated in an AD model. In this study, we investigated the anti-inflammatory effects of M. arvensis essential oil (MAEO) and its underlying molecular mechanism in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and HaCaT cells (human epidermal keratinocyte). Additionally, we examined the ameliorating effects of the MAEO in a dinitrochlorobenzene (DNCB)-induced murine model of AD. We found, in both RAW 264.7 cells and HaCaT cells, MAEO inhibited LPS-stimulated inflammatory mediators such as nitric oxide (NO) and prostaglandin E2 and proinflammatory cytokines, including IL-1β and IL-6, due to the suppression of COX-2 and iNOS expression. In LPS-stimulated macrophages, we also observed that MAEO inhibited the phosphorylation of ERK and P65. Furthermore, MAEO treatment attenuated AD symptoms, including the dermatitis score, ear thickness, epidermal thickness and infiltration of mast cells, in a DNCB-induced animal model of AD. Overall, our findings suggest that MAEO exerts anti-inflammatory and anti-atopic dermatitis effects via inhibition of the ERK/NF-κB signaling pathway. Full article
(This article belongs to the Special Issue Oxidative Damage in Korean Medicine)
►▼ Show Figures

Figure 1

20 pages, 5384 KiB  
Article
Peucedanum japonicum Thunberg and Its Active Components Mitigate Oxidative Stress, Inflammation and Apoptosis after Urban Particulate Matter-Induced Ocular Surface Damage
by Wan Seok Kang, Hakjoon Choi, Ki Hoon Lee, Eun Kim, Kyeong Jo Kim, Jin Seok Kim, Chang-Su Na and Sunoh Kim
Antioxidants 2021, 10(11), 1717; https://doi.org/10.3390/antiox10111717 - 28 Oct 2021
Cited by 7 | Viewed by 1862
Abstract
We previously demonstrated that urban particulate matter (UPM) exposure decreases the migration activity and survival of human corneal epithelial cells (HCECs). Herein, we investigated the potential to improve the corneal wound-healing ability of Peucedanum japonicum Thunb. leaf extract (PJE) and its active components [...] Read more.
We previously demonstrated that urban particulate matter (UPM) exposure decreases the migration activity and survival of human corneal epithelial cells (HCECs). Herein, we investigated the potential to improve the corneal wound-healing ability of Peucedanum japonicum Thunb. leaf extract (PJE) and its active components on UPM-induced ocular surface damage in vitro and in vivo. PJE effectively assisted wound healing without altering HCEC survival and enhanced catalase (CAT), heme oxygenase 1 (HO1) and glutathione peroxidase 1 (GPX1) antioxidant gene expression. A corneal wound was uniformly induced on the right eye in all experimental animals and divided into eight groups such as two control groups (wounded right eye group—NR and non-wounded left eye group—NL), UPM treated group and PJEs (25, 50, 100, 200, 400 mg/kg) treated groups. Corneal abrasion model rats exposed to UPM showed delayed wound healing compared to unexposed rats, but wound healing was dose-dependently enhanced by PJE oral administration. Seventy-two hours after wound generation, inflammatory cells, apoptotic cells and interleukin-6 (IL-6) expression were increased substantially after UPM exposure, but PJE treatment significantly reduced the wound to an almost normal level while enhancing re-epithelialization without changing corneal thickness. Next, we tried to identify the key molecules for enhancing wound healing through fractionation. The major compounds in the fraction, confirmed by high-performance liquid chromatography (HPLC), were chlorogenic acid (CA), neochlorogenic acid (NCA) and cryptochlorogenic acid (CCA). Each type of CA isomers showed slightly different half maximal effective (EC50) and maximal effective (ECmax) concentrations, and their mixtures synergistically enhanced HCEC migration. Thus, corneal abrasion wound recovery after UPM exposure improved after PJE treatment, and the active PJE components were identified, providing an important basis to develop therapeutics for ocular surface damage using PJE. Full article
(This article belongs to the Special Issue Oxidative Damage in Korean Medicine)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-7
Back to TopTop