scholarly journals Plant Extracts as Possible Agents for Sequela of Cancer Therapies and Cachexia

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 836 ◽  
Author(s):  
Jinjoo Lee ◽  
Myung In Jeong ◽  
Hyo-Rim Kim ◽  
Hyejin Park ◽  
Won-Kyoung Moon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Plant Extracts ◽  
Cell Damage ◽  
Antioxidant Properties ◽  
B Cell Lymphoma ◽  
Cancer Therapies ◽  
Cancer Proliferation ◽  
Monocyte Chemoattractant Protein 1 ◽  
Radiation Induced ◽  
Factor Α

Cancer is a leading cause of the death worldwide. Since the National Cancer Act in 1971, various cancer treatments were developed including chemotherapy, surgery, radiation therapy and so forth. However, sequela of such cancer therapies and cachexia are problem to the patients. The primary mechanism of cancer sequela and cachexia is closely related to reactive oxygen species (ROS) and inflammation. As antioxidant properties of numerous plant extracts have been widely reported, plant-derived drugs may have efficacy on managing the sequela and cachexia. In this study, recent seventy-four studies regarding plant extracts showing ability to manage the sequela and cachexia were reviewed. Some plant-derived antioxidants inhibited cancer proliferation and inflammation after surgery and others prevented chemotherapy-induced normal cell apoptosis. Also, there are plant extracts that suppressed radiation-induced oxidative stress and cell damage by elevation of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and regulation of B-cell lymphoma 2 (BcL-2) and Bcl-2-associated X protein (Bax). Cachexia was also alleviated by inhibition of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) by plant extracts. This review focuses on the potential of plant extracts as great therapeutic agents by controlling oxidative stress and inflammation.

scholarly journals Ethanol Extract of Maclura tricuspidata Fruit Protects SH-SY5Y Neuroblastoma Cells against H2O2-Induced Oxidative Damage via Inhibiting MAPK and NF-κB Signaling

2021 ◽  
Vol 22 (13) ◽  
pp. 6946
Author(s):  
Weishun Tian ◽  
Suyoung Heo ◽  
Dae-Woon Kim ◽  
In-Shik Kim ◽  
Dongchoon Ahn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Oxidative Damage ◽  
Cell Damage ◽  
Antioxidant Properties ◽  
Radical Scavenging ◽  
Biologically Active ◽  
Mitogen Activated Protein Kinase ◽  
Protective Effects ◽  
Neuroprotective Effects

Free radical generation and oxidative stress push forward an immense influence on the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. Maclura tricuspidata fruit (MT) contains many biologically active substances, including compounds with antioxidant properties. The current study aimed to investigate the neuroprotective effects of MT fruit on hydrogen peroxide (H2O2)-induced neurotoxicity in SH-SY5Y cells. SH-SY5Y cells were pretreated with MT, and cell damage was induced by H2O2. First, the chemical composition and free radical scavenging properties of MT were analyzed. MT attenuated oxidative stress-induced damage in cells based on the assessment of cell viability. The H2O2-induced toxicity caused by ROS production and lactate dehydrogenase (LDH) release was ameliorated by MT pretreatment. MT also promoted an increase in the expression of genes encoding the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). MT pretreatment was associated with an increase in the expression of neuronal genes downregulated by H2O2. Mechanistically, MT dramatically suppressed H2O2-induced Bcl-2 downregulation, Bax upregulation, apoptotic factor caspase-3 activation, Mitogen-activated protein kinase (MAPK) (JNK, ERK, and p38), and Nuclear factor-κB (NF-κB) activation, thereby preventing H2O2-induced neurotoxicity. These results indicate that MT has protective effects against H2O2-induced oxidative damage in SH-SY5Y cells and can be used to prevent and protect against neurodegeneration.

Epicatechin and its in vivo metabolite, 3′-O-methyl epicatechin, protect human fibroblasts from oxidative-stress-induced cell death involving caspase-3 activation

2001 ◽  
Vol 354 (3) ◽  
pp. 493-500 ◽  
Author(s):  
Jeremy P. E. SPENCER ◽  
Hagen SCHROETER ◽  
Gunter KUHNLE ◽  
S. Kaila S. SRAI ◽  
Rex M. TYRRELL ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cell Death ◽  
Caspase 3 ◽  
Cell Damage ◽  
Protective Action ◽  
Human Fibroblasts ◽  
Membrane Damage ◽  
Antioxidant Properties

There is considerable current interest in the cytoprotective effects of natural antioxidants against oxidative stress. In particular, epicatechin, a major member of the flavanol family of polyphenols with powerful antioxidant properties in vitro, has been investigated to determine its ability to attenuate oxidative-stress-induced cell damage and to understand the mechanism of its protective action. We have induced oxidative stress in cultured human fibroblasts using hydrogen peroxide and examined the cellular responses in the form of mitochondrial function, cell-membrane damage, annexin-V binding and caspase-3 activation. Since one of the major metabolites of epicatechin in vivo is 3′-O-methyl epicatechin, we have compared its protective effects with that of epicatechin. The results provide the first evidence that 3′-O-methyl epicatechin inhibits cell death induced by hydrogen peroxide and that the mechanism involves suppression of caspase-3 activity as a marker for apoptosis. Furthermore, the protection elicited by 3′-O-methyl epicatechin is not significantly different from that of epicatechin, suggesting that hydrogen-donating antioxidant activity is not the primary mechanism of protection.

scholarly journals A Pilot Study Providing Evidence for a Relationship between a Composite Lifestyle Score and Risk of Higher Carotid Intima-Media Thickness: Is There a Link to Oxidative Stress?

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Neda Seyedsadjadi ◽  
Jade Berg ◽  
Ayse A. Bilgin ◽  
Ross Grant
Keyword(s):  
Oxidative Stress ◽  
Cell Damage ◽  
Interleukin 1 ◽  
Antioxidant Properties ◽  
Intima Media Thickness ◽  
Carotid Intima Media Thickness ◽  
Blood Collection ◽  
Lifestyle Behaviours ◽  
Media Thickness ◽  
Increased Risk

Lifestyle behaviours have been closely linked to the progressive cell damage associated with oxidative stress (OS) and the development of cardiovascular disease (CVD). Early detection of lifestyle-linked OS may therefore be useful in the early identification of prodromal disease. To test this hypothesis, this study assessed the relationship between a comprehensive redox balance lifestyle score (RBLS) and carotid intima-media thickness (CIMT), a recognized marker for CVD, and plasma biomarkers of OS. In a cross-sectional study design, 100 apparently healthy middle-aged participants were asked to complete a comprehensive lifestyle questionnaire, followed by DXA scanning, CIMT ultrasonography, and blood collection. The RBLS was composed of lifestyle components with pro- and antioxidant properties with a higher score indicative of lower oxidative activity. Multiple linear regression and logistic regression analysis were performed for statistical analysis. The RBLS was significantly associated with the risk for increased CIMT that was independent of conventional CVD risk factors (χ29=35.60,P≤0.001). The adjusted model explained 42.4% of the variance in CIMT. Participants with RBLS below the median were at significantly increased risk of higher CIMT compared to participants with RBLS above the median (OR=3.60, 95% CI: 1.19–10.88,P=0.023). Significant associations were also observed between the RBLS, plasma total antioxidant capacity (TAC) (r99=0.28,P=0.006), hydroperoxide (HPX) (rs99=−0.28,P=0.005), TAC/HPX ratio (r98=0.41,P≤0.001),γ-glutamyltransferase (r97=−0.23,P=0.024), uric acid (r98=−0.20,P=0.045), and inflammatory C-reactive protein (rs97=−0.25,P=0.012) and interleukin-1β(r97=−0.21,P=0.040). These findings highlight the importance of identifying the collective influence of lifestyle behaviours on OS activity and its potential to remodel the vascular endothelium.

Catechins attenuate eccentric exercise-induced inflammation and loss of force production in muscle in senescence-accelerated mice

2011 ◽  
Vol 111 (6) ◽  
pp. 1654-1663 ◽  
Author(s):  
Satoshi Haramizu ◽  
Noriyasu Ota ◽  
Tadashi Hase ◽  
Takatoshi Murase
Keyword(s):  
Oxidative Stress ◽  
Eccentric Exercise ◽  
Inflammatory Mediators ◽  
Reductase Activity ◽  
Force Production ◽  
Monocyte Chemoattractant Protein 1 ◽  
Downhill Running ◽  
Exercise Induced ◽  
Factor Α

Catechins have a great variety of biological actions. We evaluated the potential benefits of catechin ingestion on muscle contractile properties, oxidative stress, and inflammation following downhill running, which is a typical eccentric exercise, in senescence-accelerated prone mice (SAMP). Downhill running (13 m/min for 60 min; 16° decline) induced a greater decrease in the contractile force of soleus muscle and in Ca2+-ATPase activity in SAMP1 compared with the senescence-resistant mice (SAMR1). Moreover, compared with SAMR1, SAMP1 showed greater downhill running-induced increases in plasma CPK and LDH activity, malondialdehyde, and carbonylated protein as markers of oxidative stress; and in protein and mRNA expression levels of the inflammatory mediators such as tumor necrosis factor-α and monocyte chemoattractant protein-1 in muscle. SAMP1 exhibited aging-associated vulnerability to oxidative stress and inflammation in muscle induced by downhill running. Long-term (8 wk) catechin ingestion significantly attenuated the downhill running-induced decrease in muscle force and the increased inflammatory mediators in both plasma and gastrocnemius muscle. Furthermore, catechins significantly inhibited the increase in oxidative stress markers immediately after downhill running, accompanied by an increase in glutathione reductase activity. These findings suggest that long-term catechin ingestion attenuates the aging-associated loss of force production, oxidative stress, and inflammation in muscle after exercise.

Hydrogen therapy attenuates irradiation-induced lung damage by reducing oxidative stress

2011 ◽  
Vol 301 (4) ◽  
pp. L415-L426 ◽  
Author(s):  
Yasuhiro Terasaki ◽  
Ikuroh Ohsawa ◽  
Mika Terasaki ◽  
Mikiko Takahashi ◽  
Shinobu Kunugi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Damage ◽  
A549 Cells ◽  
Lung Damage ◽  
Epithelial Cell Line ◽  
Type Iii Collagen ◽  
Treatment Groups ◽  
Human Lung Epithelial Cell ◽  
Spin Resonance ◽  
Radiation Induced

Molecular hydrogen (H2) is an efficient antioxidant that diffuses rapidly across cell membranes, reduces reactive oxygen species (ROS), such as hydroxyl radicals and peroxynitrite, and suppresses oxidative stress-induced injury in several organs. ROS have been implicated in radiation-induced damage to lungs. Because prompt elimination of irradiation-induced ROS should protect lung tissue from damaging effects of irradiation, we investigated the possibility that H2 could serve as a radioprotector in the lung. Cells of the human lung epithelial cell line A549 received 10 Gy irradiation with or without H2 treatment via H2-rich PBS or medium. We studied the possible radioprotective effects of H2 by analyzing ROS and cell damage. Also, C57BL/6J female mice received 15 Gy irradiation to the thorax. Treatment groups inhaled 3% H2 gas and drank H2-enriched water. We evaluated acute and late-irradiation lung damage after H2 treatment. H2 reduced the amount of irradiation-induced ROS in A549 cells, as shown by electron spin resonance and fluorescent indicator signals. H2 also reduced cell damage, measured as levels of oxidative stress and apoptotic markers, and improved cell viability. Within 1 wk after whole thorax irradiation, immunohistochemistry and immunoblotting showed that H2 treatment reduced oxidative stress and apoptosis, measures of acute damage, in the lungs of mice. At 5 mo after irradiation, chest computed tomography, Ashcroft scores, and type III collagen deposition demonstrated that H2 treatment reduced lung fibrosis (late damage). This study thus demonstrated that H2 treatment is valuable for protection against irradiation lung damage with no known toxicity.

Empetrum nigrum var. japonicum Extract Suppresses γ-Ray Radiation-Induced Cell Damage via Inhibition of Oxidative Stress

2011 ◽  
Vol 39 (01) ◽  
pp. 161-170 ◽  
Author(s):  
Ki Cheon Kim ◽  
In Kyung Lee ◽  
Kyoung Ah Kang ◽  
Bum Joon Kim ◽  
Daeshin Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Modification ◽  
Cell Damage ◽  
Membrane Lipid ◽  
Mitogen Activated Protein Kinase ◽  
Γ Radiation ◽  
Empetrum Nigrum ◽  
Mitogen Activated Protein ◽  
Radiation Induced ◽  
Cellular Dna

The ethylacetate fraction of Empetrum nigrum var. japonicum (ENE) was shown to reduce intracellular reactive oxygen species (ROS) generated by γ-radiation and activate antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and gluthathion peroxidase (GPx). ENE protected cells against radiation-induced cellular DNA damage, membrane lipid peroxidation, and protein modification, which are the main points of radiation-induced damage. In addition, ENE recovered cell viability by inhibiting apoptosis after cells were treated with radiation. ENE treatment also reduced γ-radiation induced Bax, and caspase 9 and 3 expression in irradiated cells. However, irradiated cells with ENE recovered Bcl-2 expression, which was reduced by radiation. This anti-apoptotic effect of ENE was due to the inhibition of mitogen-activated protein kinase kinase-4 (MKK4/SEK1)-c-Jun NH2-terminal kinase (JNK) cascades induced by γ-radiation. In summary, these results suggest that ENE protects cells against γ-radiation-induced oxidative stress via the reduction of ROS and attenuation of apoptosis.

scholarly journals Human Relaxin-2 (Serelaxin) Attenuates Oxidative Stress in Cardiac Muscle Cells Exposed In Vitro to Hypoxia–Reoxygenation. Evidence for the Involvement of Reduced Glutathione Up-Regulation

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 774
Author(s):  
Silvia Nistri ◽  
Claudia Fiorillo ◽  
Matteo Becatti ◽  
Daniele Bani
Keyword(s):  
Oxidative Stress ◽  
Cardiac Muscle ◽  
Reduced Glutathione ◽  
Cell Damage ◽  
Antioxidant Properties ◽  
Muscle Cells ◽  
Protective Effects ◽  
Cardiac Muscle Cells ◽  
Relaxin 2

Serelaxin (RLX) designates the pharmaceutical form of the human natural hormone relaxin-2 that has been shown to markedly reduce tissue and cell damage induced by hypoxia and reoxygenation (HR). The evidence that RLX exerts similar protective effects on different organs and cells at relatively low, nanomolar concentrations suggests that it specifically targets a common pathogenic mechanism of HR-induced damage, namely oxidative stress. In this study we offer experimental evidence that RLX (17 nmol L-1), added to the medium of HR-exposed H9c2 rat cardiac muscle cells, significantly reduces cell oxidative damage, mitochondrial dysfunction and apoptosis. These effects appear to rely on the up-regulation of the cellular availability of reduced glutathione (GSH), a ubiquitous endogenous antioxidant metabolite. Conversely, superoxide dismutase activity was not influenced by RLX, which, however, was not endowed with chemical antioxidant properties. Taken together, these findings verify the major pharmacological role of RLX in the protection against HR-induced oxidative stress, and shed first light on its mechanisms of action.

Interactions between oxidative stress and inflammation in salt-sensitive hypertension

2007 ◽  
Vol 293 (6) ◽  
pp. H3388-H3395 ◽  
Author(s):  
N. Tian ◽  
R. S. Moore ◽  
S. Braddy ◽  
R. A. Rose ◽  
J.-W. Gu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Arterial Pressure ◽  
Renal Plasma Flow ◽  
Nuclear Factor Κb ◽  
Antioxidant Treatment ◽  
Monocyte Chemoattractant Protein 1 ◽  
Cytokines And Chemokines ◽  
Protein Excretion ◽  
Factor Α ◽  
Salt Sensitive Hypertension

The goal of this study was to test the hypothesis that increases in oxidative stress in Dahl S rats on a high-salt diet help to stimulate renal nuclear factor-κB (NF-κB), renal proinflammatory cytokines, and chemokines, thus contributing to hypertension, renal damage, and dysfunction. We specifically studied whether antioxidant treatment of Dahl S rats on high Na intake would decrease renal inflammation and thus attenuate the hypertensive and adverse renal responses. Sixty-four 7- to 8-wk-old Dahl S or R/Rapp strain rats were maintained for 5 wk on high Na (8%) or high Na + vitamins C (1 g/l in drinking water) and E (5,000 IU/kg in food). Arterial and venous catheters were implanted at day 21. By day 35 in the high-Na S rats, antioxidant treatment significantly increased the renal reduced-to-oxidized glutathione ratio and decreased renal cortical H2O2 and O2•− release and renal NF-κB. Antioxidant treatment with vitamins C and E in high-Na S rats also decreased renal monocytes/macrophages in the glomeruli, cortex, and medulla, decreased tumor necrosis factor-α by 39%, and decreased monocyte chemoattractant protein-1 by 38%. Vitamin-treated, high-Na S rats also experienced decreases in arterial pressure, urinary protein excretion, renal tubulointerstitial damage, and glomerular necrosis and increases in glomerular filtration rate and renal plasma flow. In conclusion, antioxidant treatment of high-Na Dahl S rats decreased renal inflammatory cytokines and chemokines, renal immune cells, NF-κB, and arterial pressure and improved renal function and damage.

Phloroglucinol (1,3,5-trihydroxybenzene) protects against ionizing radiation-induced cell damage through inhibition of oxidative stress in vitro and in vivo

2010 ◽  
Vol 185 (3) ◽  
pp. 215-226 ◽  
Author(s):  
Kyoung Ah Kang ◽  
Rui Zhang ◽  
Sungwook Chae ◽  
Su Jae Lee ◽  
Jihoon Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ionizing Radiation ◽  
Cell Damage ◽  
Radiation Induced
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