Protective effect of the methanolic extract from Duchesnea indica against oxidative stress in vitro and in vivo

Weicheng Hu; Woong Han; Chaoqing Huang; Myeong-Hyeon Wang

doi:10.1016/j.etap.2010.09.004

miR-187 modulates cardiomyocyte apoptosis and oxidative stress in myocardial infarction mice via negatively regulating DYRK2

10.22514/sv.2021.137 ◽

2021 ◽

Keyword(s):

Oxidative Stress ◽

Myocardial Infarction ◽

Protective Effect ◽

Myocardial Infarct ◽

Annexin V ◽

Cardiomyocyte Apoptosis ◽

Ros Generation ◽

Downstream Target

Myocardial infarction is a serious representation of cardiovescular disease, MicroRNAs play a role in modifying I/R injury and myocardial infarct remodeling. The present study therefore examined the potential role of miR-187 in cardiac I/R injury and its underlying mechanisms. miR-187 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with miR-187 mimic or inhibitor to confirm the function of miR-187 in H/R. DYRK2 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with DYRK2 inhibitor. A myocardium I/R mouse model was established. Circulating levels of miR-187 or DYRK2 was detected by quantitative realtime PCR and protein expression was detected by western blotting. The cell viability in all groups was determined by MTT assay and the apoptosis ratio was detected by flow cytometry after staining with Annexin V-FITC. The effect of miR-187 on cellular ROS generation was examined by DCFH-DA. The level of lipid peroxidation and SOD expression were determined by MDA and SOD assay. The findings indicated that miR-187 may be a possible regulator in the protective effect of H/R-induced cardiomyocyte apoptosis, cellular oxidative stress and leaded to DYRK2 suppression at a posttranscriptional level. Moreover, the improvement of miR-187 on H/R-induced cardiomyocyte injury contributed to the obstruction of DYRK2 expression. In addition, these results identified DYRK2 as the functional downstream target of miR-187 regulated myocardial infarction and oxidative stress.These present work provided the first insight into the function of miR-187 in successfully protect cardiomyocyte both in vivo and in vitro, and such a protective effect were mediated through the regulation of DYRK2 expression.

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Protective effect of quercetin in gentamicin-induced oxidative stress in vitro and in vivo in blood cells. Effect on gentamicin antimicrobial activity

Environmental Toxicology and Pharmacology ◽

10.1016/j.etap.2016.11.004 ◽

2016 ◽

Vol 48 ◽

pp. 253-264 ◽

Cited By ~ 18

Author(s):

Pamela Soledad Bustos ◽

Romina Deza-Ponzio ◽

Paulina Laura Páez ◽

Ines Albesa ◽

José Luis Cabrera ◽

...

Keyword(s):

Oxidative Stress ◽

Antimicrobial Activity ◽

Protective Effect ◽

Blood Cells

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Inhibitory effects of Panax ginseng glycoproteins in models of doxorubicin-induced cardiac toxicity in vivo and in vitro

Food & Function ◽

10.1039/d1fo01307f ◽

2021 ◽

Author(s):

Yajun Chen ◽

Lei Wang ◽

Tianjia Liu ◽

Zhidong Qiu ◽

Ye Qiu ◽

...

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

Cell Viability ◽

Panax Ginseng ◽

Cardiac Toxicity ◽

H9c2 Cell ◽

Inhibitory Effects ◽

Myocardial Oxidative Stress

We investigated the protective effect of PGP against DOX-induced cardiotoxicity in vitro and in vivo. PGP increases H9C2 cell viability and inhibits apoptosis, alleviating DOX-induced myocardial oxidative stress-related cardiotoxicity.

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Protective Effect of Hydroxytyrosol Against Oxidative Stress Induced by the Ochratoxin in Kidney Cells: in vitro and in vivo Study

Frontiers in Veterinary Science ◽

10.3389/fvets.2020.00136 ◽

2020 ◽

Vol 7 ◽

Cited By ~ 3

Author(s):

Rosalia Crupi ◽

Ernesto Palma ◽

Rosalba Siracusa ◽

Roberta Fusco ◽

Enrico Gugliandolo ◽

...

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

In Vivo Study ◽

Kidney Cells

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In Vitro and In Vivo Inhibitory Effect of Citrus Junos Tanaka Peel Extract against Oxidative Stress-Induced Apoptotic Death of Lung Cells

Antioxidants ◽

10.3390/antiox9121231 ◽

2020 ◽

Vol 9 (12) ◽

pp. 1231

Author(s):

Jin Woo Kim ◽

Eun Hee Jo ◽

Ji Eun Moon ◽

Hanvit Cha ◽

Moon Han Chang ◽

...

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

Inhibitory Effect ◽

Lung Cells ◽

In Vivo Models ◽

Citrus Junos ◽

Induced Apoptosis ◽

Peel Extract

Various stresses derived from both internal and external oxidative environments lead to the excessive production of reactive oxygen species (ROS) causing progressive intracellular oxidative damage and ultimately cell death. The objective of this study was to evaluate the protective effects of Citrus junos Tanaka peel extract (CE) against oxidative-stress induced the apoptosis of lung cells and the associated mechanisms of action using in vitro and in vivo models. The protective effect of CE was evaluated in vitro in NCI-H460 human lung cells exposed to pro-oxidant H2O2. The preventive effect of CE (200 mg/kg/day, 10 days) against pulmonary injuries following acrolein inhalation (10 ppm for 12 h) was investigated using an in vivo mouse model. Herein, we demonstrated the inhibitory effect of CE against the oxidative stress-induced apoptosis of lung cells under a highly oxidative environment. The function of CE is linked with its ability to suppress ROS-dependent, p53-mediated apoptotic signaling. Furthermore, we evaluated the protective role of CE against apoptotic pulmonary injuries associated with the inhalation of acrolein, a ubiquitous and highly oxidizing environmental respiratory pollutant, through the attenuation of oxidative stress. The results indicated that CE exhibits a protective effect against the oxidative stress-induced apoptosis of lung cells in both in vitro and in vivo models.

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Protective Effect of Coconut Oil Meal Phenolic Antioxidants against Macromolecular Damage: In Vitro and In Vivo Study

Journal of Chemistry ◽

10.1155/2020/3503165 ◽

2020 ◽

Vol 2020 ◽

pp. 1-8 ◽

Cited By ~ 1

Author(s):

A. N. Karunasiri ◽

C. M. Senanayake ◽

H. Hapugaswatta ◽

N. Jayathilaka ◽

K. N. Seneviratne

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

Stress Responses ◽

Coconut Oil ◽

Oral Feeding ◽

Phenolic Antioxidants ◽

Significant Difference ◽

Macromolecular Damage

Coconut oil meal, a cheap by-product of coconut oil production, is a rich source of phenolic antioxidants. Many age-related diseases are caused by reactive oxygen species- (ROS-) induced damage to macromolecules such as lipids, proteins, and DNA. In the present study, the protective effect of the phenolic extract of coconut oil meal (CMPE) against macromolecular oxidative damage was evaluated using in vitro and in vivo models. Sunflower oil, bovine serum albumin (BSA), and plasmid DNA were used in the in vitro study, and thiobarbituric acid reactive substances (TBARS), protein carbonyl, and nicked DNA were evaluated as oxidation products. The inhibitory effect of CMPE against H2O2-induced macromolecular damage was evaluated using cultured HEp-2 cells. The results indicate that CMPE inhibits macromolecular damage both in vitro and in vivo. In addition, CMPE regulates redox status of HEp-2 cells under oxidative stress conditions by maintaining higher reduced glutathione levels. There was no significant difference in the expression of glutathione peroxidase in stressed and unstressed cells suggesting that CMPE regulates the cellular oxidative stress responses without affecting the expression of oxidative stress response genes. Oral feeding of Wistar rats with CMPE improves the serum and plasma antioxidant status without causing any toxic effects.

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Protective Effect of Liposome-Encapsulated Glutathione in a Human Epidermal Model Exposed to a Mustard Gas Analog

Journal of Toxicology ◽

10.1155/2011/109516 ◽

2011 ◽

Vol 2011 ◽

pp. 1-11 ◽

Cited By ~ 17

Author(s):

Victor Paromov ◽

Sudha Kumari ◽

Marianne Brannon ◽

Naga S. Kanaparthy ◽

Hongsong Yang ◽

...

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

Cell Viability ◽

Sulfur Mustard ◽

Alkylating Agents ◽

Water Soluble ◽

Model Systems ◽

Mustard Gas

Sulfur mustard or mustard gas (HD) and its monofunctional analog, 2-chloroethyl ethyl sulfide (CEES), or “half-mustard gas,” are alkylating agents that induce DNA damage, oxidative stress, and inflammation. HD/CEES are rapidly absorbed in the skin causing extensive injury. We hypothesize that antioxidant liposomes that deliver both water-soluble and lipid-soluble antioxidants protect skin cells from immediate CEES-induced damage via attenuating oxidative stress. Liposomes containing water-soluble antioxidants and/or lipid-soluble antioxidants were evaluated usingin vitromodel systems. Initially, we found that liposomes containing encapsulated glutathione (GSH-liposomes) increased cell viability and attenuated production of reactive oxygen species (ROS) in HaCaT cells exposed to CEES. Next, GSH-liposomes were tested in a human epidermal model, EpiDerm. In the EpiDerm, GSH-liposomes administered simultaneously or 1 hour after CEES exposure (2.5 mM) increased cell viability, inhibited CEES-induced loss of ATP and attenuated changes in cellular morphology, but did not reduce caspase-3 activity. These findings paralleled the previously describedin vivoprotective effect of antioxidant liposomes in the rat lung and established the effectiveness of GSH-liposomes in a human epidermal model. This study provides a rationale for use of antioxidant liposomes against HD toxicity in the skin considering further verification in animal models exposed to HD.

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